HIPERTENSION ARTERIAL Y ARRITMIAS

HIPERTENSION ARTERIAL Y ARRITMIAS
José Luis Serra Jefe Area de Arritmias y Marcapasos Sanatorio Allende Hospital Córdoba

The 7 pathways in the progression from hypertension to heart failure
The 7 pathways in the progression from hypertension to heart failure. Hypertension progresses to concentric (thick-walled) LVH (cLVH; pathway 1). The direct pathway from hypertension to dilated cardiac failure (increased LV volume with reduced LVEF) can occur without (pathway 2) or with (pathway 3) an interval myocardial infarction (MI). Concentric hypertrophy progresses to dilated cardiac failure (transition to failure) most commonly via an interval myocardial infarction (pathway 4). Recent data suggest that it is not common for concentric hypertrophy to progress to dilated cardiac failure without interval myocardial infarction (pathway 5). Patients with concentric LVH can develop symptomatic heart failure with a preserved LVEF (pathway 6), and patients with dilated cardiac failure can develop symptomatic heart failure with reduced LVEF (pathway 7). The influences of other important modulators of the progression of hypertensive heart disease, including obesity, diabetes mellitus, age, environmental exposures, and genetic factors, are not shown to simplify the diagram. A thicker arrow depicts a more common pathway compared with a thinner arrow. Adapted from Drazner.2 Copyright 2005 ©, the American Heart Association. Circulation 2011;123:

CARDIOPATIA HIPERTENSIVA
Patología de HVI Hipertrofia del miocito Fibroblastos: hiperplasian, en miofibroblastos Expansion de colágeno intersticial y perivascular Hipertrofia de celulas musculares lisas de la pared vascular Cambios en densidad capilar intramiocárdica Engrosamiento arteriolar Cardiomyocyte hypertrophy is but one of many structural alterations in HHD(5). Fibroblasts undergo hyperplasia and conversion to myofibroblasts, along with hypertrophy of vascular smooth muscle cells. Noncellular elements central to myocardial remodeling in HHD include expansion of interstitial and perivascular collagen that make up the extracellular matrix. Changes in intramyocardial capillary density and arteriolar thickening compound ischemia in the hearts of patients with hypertension

Mecanismos responsables de la HVI Sobrecarga Neurohormonas: SRAA-A, Catecolaminas Factores de crecimiento Citokinas GENETICA

En HTA ocurre con mas frecuencia: Sin HVI: Ligero incremento de ESV y EVs Con HVI: Fibrilación Auricular: su incidencia aumenta 40 a 50 % Arritmia Ventricular: incremento hasta 9 veces FV / MS: mas frecuencia (31 vs 10 %) 2. Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol 1998;82:2N–9N. 4. Dimopoulos S, Nicosia F, Donati P, et al. QT dispersion and left ventricular hypertrophy in elderly hypertensive and normotensive patients. Angiology 2008;59:605–12. [PubMed: ] Comentarios Messerli et al [21] reported on a small increase of supraventricular and ventricular tachyarrhythmias in hypertensive patients without evidence of LVH, compared to the general population. However, in the hypertensive individuals with LVH, the risk for both types of tachyarrhythmias increased by more than 9-fold. In the same study, frequent polymorphic and repetitive ventricular arrhythmias occurred only in patients with LVH. Moreover, hypertensive patients with LVH are significantly more prone to experience ventricular fibrillation or sudden death than those without LVH (31% v 10%), despite absence of documented coronary artery disease [22]. Current Pharmaceutical Design, 2011, 17, /11 $ © 2011 Bentham Science Publishers Markers of Arrhythmogenic Risk in Hypertensive Subjects Andrea Barison1,2, Giuseppe Vergaro1, Luigi Emilio Pastormerlo1, Lorenzo Ghiadoni3, Michele Emdin1 and Claudio Passino1,2,* 1Fondazione “G. Monasterio” CNR - Regione Toscana, Pisa, Italy, 2Scuola Superiore Sant’Anna, Pisa, Italy, 3Department of Internal Medicine, University of Pisa, Pisa, Italy Abstract: Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias.

MECANISMOS ARRITMOGENICOS EN LA HIPERTROFIA
Determinants of ventricular arrhythmias in cardiac hypertrophy. J Cardiovasc Pharmacol. 1991;17 Suppl 2:S46-9 Abstract McLenachan JM, Dargie HJ. Ventricular arrhythmias occur with increased frequency in both experimental and human cardiac hypertrophy. Although the process of hypertrophy itself may be arrhythmogenic, other factors may contribute to the high prevalence of arrhythmias in hypertensive patients with left ventricular hypertrophy (LVH). Disease of the large epicardial coronary arteries or of the small intramyocardial vessels (coronary microangiopathy) may lead to myocardial ischemia and thus predispose to arrhythmia. Myocardial fibrosis, a common sequelae of cardiac hypertrophy, has also been shown to be associated with ventricular arrhythmias in experimental models. Other possible determinants of ventricular arrhythmias in this group of patients include metabolic abnormalities; studies relating to the importance of hypokalemia in particular have yielded conflicting results. Thus a number of factors may combine to explain the high prevalence of ventricular arrhythmias in hypertensive patients with LVH. Otros comentarios Control of the sudden blood pressure increase had protective effect against arrhythmias in both experimental and clinical settings [11 Shortening of the monophasic action potential or refractory period or the QT interval upon loading the myocardium (or their lengthening with unloading), or opposite effects, depending on the experimental conditions, have been observed The interpretation of these results is complicated by the fact that both shortening of refractoriness (favouring early re-excitation and reentry) and prolongation of refractoriness (associated with repolarisation and triggered activity) may be arrhythmogenic Dispersion of the electrophysiological properties between adjacent areas may be a more plausible explanation of hypertension-induced arrhythmias

HIPERTROFIA VENTRICULAR
Current Pharmaceutical Design, 2011, 17, /11 $ © 2011 Bentham Science Publishers Markers of Arrhythmogenic Risk in Hypertensive Subjects Andrea Barison1,2, Giuseppe Vergaro1, Luigi Emilio Pastormerlo1, Lorenzo Ghiadoni3, Michele Emdin1 and Claudio Passino1,2,* 1Fondazione “G. Monasterio” CNR - Regione Toscana, Pisa, Italy, 2Scuola Superiore Sant’Anna, Pisa, Italy, 3Department of Internal Medicine, University of Pisa, Pisa, Italy Abstract: Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias.

Schematic Illustrating How Fibrosis Disrupts Myocyte Coupling
Figure 2 Schematic Illustrating How Fibrosis Disrupts Myocyte Coupling Cardiomyocytes in normal myocardial tissue (A) are electrically coupled primarily in an end-to-end fashion by intercellular gap-junctional complexes. Reactive fibrosis results in extracellular matrix expansion between bundles of myocytes (B), while reparative fibrosis replaces degenerating myocytes (C). Both patterns of collagen distribution become exaggerated during structural remodeling. Figure illustration by Rob Flewell. Myocyte loss, either by apoptosis or necrosis (9,26), is observed in parallel with the onset of fibrosis. Reparative fibrosis replaces degenerating myocardial cells (33), whereas coexisting reactive fibrosis causes interstitial expansion between bundles of myocytes (7,34), as shown in Figure 2. Pathologically produced collagen differs from that in normal myocardium, with altered ratios of collagen subtypes (20,35). Dense and disorganized collagen weave fibrils physically separate remaining myocytes (36), and can create a barrier to impulse propagation. Fibrosis interferes with conduction by impairing intermyocyte coupling. Myocardial electrical continuity is maintained by specialized proteins called connexins located in gap junctions, which form cell-to-cell connections that maintain low-resistance intercellular coupling. Alterations in ventricular expression and function of the major cardiac connexin, connexin 43, are observed in CHF and correlate with proarrhythmic conduction slowing (37). Hypophosphorylation of connexins and their redistribution to lateral cell borders are the salient features (37,38), with connexin disorganization correlating with fibrosis (39). Studies of gap-junctional remodeling in the atria have produced discrepant results (40), and changes may depend on the degree and/or type of underlying pathology (41). Atrial gap junction remodeling seems to reverse slowly (42), but it is still unclear how much connexin disruption is required to observe an effect on conduction. Schematic Illustrating How Fibrosis Disrupts Myocyte Coupling J Am Coll Cardiol 2008;51:

MECANISMOS ARRITMOGENICOS EN LA HIPERTROFIA
Fibrosis miocárdica Enfermedade coronaria Microangiopatía Disbalance oferta /demanda Disbalances neurovegetativos Picos hipertensivos Anormalidades metabólicas, hipokalemia Alteraciones en la: Conducción Despolarización Repolarización Automatismo aumentado Actividad gatillada Determinants of ventricular arrhythmias in cardiac hypertrophy. J Cardiovasc Pharmacol. 1991;17 Suppl 2:S46-9 Abstract McLenachan JM, Dargie HJ. Ventricular arrhythmias occur with increased frequency in both experimental and human cardiac hypertrophy. Although the process of hypertrophy itself may be arrhythmogenic, other factors may contribute to the high prevalence of arrhythmias in hypertensive patients with left ventricular hypertrophy (LVH). Disease of the large epicardial coronary arteries or of the small intramyocardial vessels (coronary microangiopathy) may lead to myocardial ischemia and thus predispose to arrhythmia. Myocardial fibrosis, a common sequelae of cardiac hypertrophy, has also been shown to be associated with ventricular arrhythmias in experimental models. Other possible determinants of ventricular arrhythmias in this group of patients include metabolic abnormalities; studies relating to the importance of hypokalemia in particular have yielded conflicting results. Thus a number of factors may combine to explain the high prevalence of ventricular arrhythmias in hypertensive patients with LVH. Otros comentarios Control of the sudden blood pressure increase had protective effect against arrhythmias in both experimental and clinical settings [11 Shortening of the monophasic action potential or refractory period or the QT interval upon loading the myocardium (or their lengthening with unloading), or opposite effects, depending on the experimental conditions, have been observed The interpretation of these results is complicated by the fact that both shortening of refractoriness (favouring early re-excitation and reentry) and prolongation of refractoriness (associated with repolarisation and triggered activity) may be arrhythmogenic Dispersion of the electrophysiological properties between adjacent areas may be a more plausible explanation of hypertension-induced arrhythmias

Ventricular Arrhythmias in Patients with Hypertensive Left Ventricular Hypertrophy N Engl J Med 1987; 317: Condición N. Holter. TV no S HTA con HVI (ECG) 50 (28%) * HTA sin HVI (ECG) ( 8%) * Controles, sin HTA ( 2%) Abstract In patients with hypertension, a pattern of left ventricular hypertrophy on the electrocardiogram is associated with a risk of sudden death in excess of the risk attributable to hypertension alone. We therefore investigated the frequency of complex ventricular arrhythmias by means of 48-hour ambulatory electrocardiographic monitoring in 100 treated hypertensive patients, of whom 50 had electrocardiographic evidence of left ventricular hypertrophy and 50 did not, and in 50 normotensive controls. The groups were matched for age, sex, and smoking habits, and the two hypertensive groups were matched for blood-pressure levels before and after antihypertensive therapy. Nonsustained ventricular tachycardia, defined as ≥3 complexes at a rate ≤120 beats per minute, occurred in 14 (28 percent) of the 50 patients with an electro-cardiographic pattern of left ventricular hypertrophy, in 4 (8 percent) of the 50 patients without hypertrophy (P<0.05), and in 1 (2 percent) of the control subjects. Eight of the 50 patients (16 percent) with hypertrophy had episodes of nonsustained ventricular tachycardia longer than 5 complexes, whereas no patients without hypertrophy and no controls had such episodes. The group with nonsustained ventricular tachycardia was characterized by a high left ventricular mass on echocardiography and a high prevalence of ST-T abnormalities on electrocardiography. Ventricular tachycardia was not closely related to blood-pressure levels, nor was it associated with diuretic therapy or hypokalemia. The clinical importance of these arrhythmias is uncertain. Nevertheless, our data suggest that complex ventricular arrhythmias occur commonly in hypertensive patients with left ventricular hypertrophy and may contribute to the higher incidence of sudden death in these patients. * P < 0,05

Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension Hypertension. 1996;28: 126 HTA esenciales. Holter MAPA Ecocardiograma EVs en 71% Lown ≥ 2 vs 0-1: + edad (54 vs 45 a) + tiempo de HTA (5.4 vs 2.8 a), + HVI + hipertensión nocturna Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension Giuseppe Schillaci, Paolo Verdecchia, Claudia Borgioni, Antonella Ciucci, Ivano Zampi, Massimo Battistelli, Roberto Gattobigio, Nicola Sacchi, and Carlo Porcellati Hypertension. 1996;28: , Abstract Hypertension is a risk factor for sudden cardiac death, and some data indicate that frequent and complex ventricular arrhythmias may be additional risk markers in hypertensive individuals. We investigated the relation between ventricular arrhythmias and the persistence of increased blood pressure levels over 24 hours in subjects with essential hypertension. We studied 126 never-treated subjects with essential hypertension (83 men) who underwent 24-hour electrocardiographic monitoring, 24-hour ambulatory blood pressure monitoring, and echocardiography. Premature ventricular beats were detected in 71% of the subjects. Compared with subjects in Lown class 0-1, subjects with frequent or complex ventricular arrhythmias (Lown class ≥2) were older (54 versus 45 years) and had a longer duration of hypertension (5.4 versus 2.8 years), a greater left ventricular mass (147 versus 127 g·m−2), and a blunted nocturnal reduction in ambulatory blood pressure (7%/12% versus 12%/16%). The number of premature ventricular beats over 24 hours was associated with age (r=.25), left ventricular mass (r=.24), and pulse pressure (r=.18) and inversely associated with the percent reduction in blood pressure from day to night (r=−.29 for systolic and −.25 for diastolic pressures). In a multiple logistic regression analysis, frequent or complex ventricular arrhythmias (Lown class ≥2) were predicted by an age ≥60 years (odds ratio, 10.4; 95% confidence interval, ), left ventricular hypertrophy at echocardiography (odds ratio, 4.2; 95% confidence interval, ), and a <10% reduction in blood pressure from day to night (“nondipping” pattern: odds ratio, 2.9; 95% confidence interval, ). We conclude that in addition to the strong effect of age and left ventricular hypertrophy at echocardiography, the persistence of high blood pressure levels over the 24 hours (“nondipping” pattern) is an independent predictor of the frequency and complexity of ventricular arrhythmias in never-treated subjects with essential hypertension.

Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension Hypertension. 1996;28: Total PVBs per 24 hours in 126 hypertensive subjects grouped by nocturnal BP reduction and echocardiographic LV hypertrophy (LVH). See text for details. Data are mean and SE. Association Between Persistent Pressure Overload and Ventricular Arrhythmias in Essential Hypertension Giuseppe Schillaci, Paolo Verdecchia, Claudia Borgioni, Antonella Ciucci, Ivano Zampi, Massimo Battistelli, Roberto Gattobigio, Nicola Sacchi, and Carlo Porcellati Hypertension. 1996;28: , Abstract Hypertension is a risk factor for sudden cardiac death, and some data indicate that frequent and complex ventricular arrhythmias may be additional risk markers in hypertensive individuals. We investigated the relation between ventricular arrhythmias and the persistence of increased blood pressure levels over 24 hours in subjects with essential hypertension. We studied 126 never-treated subjects with essential hypertension (83 men) who underwent 24-hour electrocardiographic monitoring, 24-hour ambulatory blood pressure monitoring, and echocardiography. Premature ventricular beats were detected in 71% of the subjects. Compared with subjects in Lown class 0-1, subjects with frequent or complex ventricular arrhythmias (Lown class ≥2) were older (54 versus 45 years) and had a longer duration of hypertension (5.4 versus 2.8 years), a greater left ventricular mass (147 versus 127 g·m−2), and a blunted nocturnal reduction in ambulatory blood pressure (7%/12% versus 12%/16%). The number of premature ventricular beats over 24 hours was associated with age (r=.25), left ventricular mass (r=.24), and pulse pressure (r=.18) and inversely associated with the percent reduction in blood pressure from day to night (r=−.29 for systolic and −.25 for diastolic pressures). In a multiple logistic regression analysis, frequent or complex ventricular arrhythmias (Lown class ≥2) were predicted by an age ≥60 years (odds ratio, 10.4; 95% confidence interval, ), left ventricular hypertrophy at echocardiography (odds ratio, 4.2; 95% confidence interval, ), and a <10% reduction in blood pressure from day to night (“nondipping” pattern: odds ratio, 2.9; 95% confidence interval, ). We conclude that in addition to the strong effect of age and left ventricular hypertrophy at echocardiography, the persistence of high blood pressure levels over the 24 hours (“nondipping” pattern) is an independent predictor of the frequency and complexity of ventricular arrhythmias in never-treated subjects with essential hypertension. Total PVBs per 24 hours in 126 hypertensive subjects grouped by nocturnal BP reduction and echocardiographic LV hypertrophy (LVH). Hypertension 1996;28:

HVI y prevalencia de Arritmia Ventricular en Hipertensos
HVI y prevalencia de Arritmia Ventricular en Hipertensos. Med Klin (Munich) Oct 15;103(10): 192 patients con HTA, HVI, sin enf coronaria. Tipo: Concéntrica, excéntrica, asimétrica Severidad : leve, moderada, severa Prevalencia de AV por Holter y ergometría Correlación Si, con severidad No, con tipo de HVI Med Klin (Munich) Oct 15;103(10): Epub 2008 Oct 21. Influence of the type and degree of left ventricular hypertrophy on the prevalence of ventricular arrhythmias in patients with hypertensive heart disease. Kunisek J, Zaputović L, Mavrić Z, Kunisek L, Bruketa-Markić I, Karlavaris R, Lukin-Eskinja K. Source Department of Cardiovascular Diseases, Health Center Rijeka, Rijeka, Croatia. Abstract PURPOSE: To investigate the correlation between the prevalence of ventricular arrhythmias (VA) and the type and degree of left ventricular hypertrophy (LVH) in hypertensive patients using exercise testing and Holter monitoring. PATIENTS AND METHODS: A total of 192 patients (87 men and 105 women) without coronary disease were divided into three groups according to type of LVH (concentric, eccentric, and asymmetric) and three subgroups in relation to the degree of hypertrophy (mild, moderate, and severe). In all subjects blood pressure was measured, electrocardiographic and echocardiographic data obtained and the prevalence of VA determined by Holter monitoring and bicycle ergometry. RESULTS: The most frequent LVH type was the concentric (63%), followed by eccentric (28%) and asymmetric (9%). Severe LVH was found in 10% of patients. Complex VA during Holter monitoring were identified in > 40% of patients. During the stress test this percentage increased by additional 7.4%. There was no statistically significant difference between groups in frequency of simple (p = 0.757) and complex (p = 0.657, p = 0.819, p = 0.617, for polytopic, pairs and ventricular tachycardia, respectively) VA. Increased prevalence of VA was found for the moderate and severe degree in all types. In the concentric type the difference was statistically significant for simple VA (p = 0.042). CONCLUSION: : There was no correlation between type of LVH and prevalence of VA. The severity of hypertrophy contributes more to a greater prevalence of VA than the LVH pattern. The combination of severe degree and concentric type carries the greatest cardiovascular risk.

HTA HVI ARRITMIA VENTRICULAR

INDICADORES DE RIESGO DE ARRITMIA y MUERTE SUBITA
Biohumorales: neurohormonas ECG: Despolarización: QRS Potenciales ventriculares tardios. Repolarización: QTc Dispersión del QT Microalternancia de la onda T Balance neurovegetativo Variabilidad de la FC Imágenes Ecocardiografía RMN Curr Pharm Des. 2011;17(28): Markers of arrhythmogenic risk in hypertensive subjects. Barison A, Vergaro G, Pastormerlo LE, Ghiadoni L, Emdin M, Passino C. Source Fondazione G. Monasterio CNR - Regione Toscana, Pisa, Italy. Abstract Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias.

Increased Left Ventricular Mass and Hypertrophy Are Associated With Increased Risk for Sudden Death J Am Coll Cardiol 1998;32:1454 –9 Framingham Heart Study 3,661 sujetos >40 a de edad 14 a de seguimiento Prevalencia de HVI: 21.5%. HR para MS = 1.45 (IC 95% = 1.10 to 1.92, p = 0.008) por cada 50-g/m de incremento en la masa VI. M.S. Increased Left Ventricular Mass and Hypertrophy Are Associated With Increased Risk for Sudden Death AGHA W. HAIDER, MD, PHD,*‡¶ MARTIN G. LARSON, SCD,*‡ EMELIA J. BENJAMIN, MD, SCM, FACC,§ DANIEL LEVY, MD, FACC*†‡§\ Boston and Framingham, Massachusetts and Bethesda, Maryland Objectives. This study examined the relations of echocardiographically determined left ventricular (LV) mass and hypertrophy to the risk of sudden death. Background. Echocardiographic LV hypertrophy is associated with increased risk for all-cause mortality and cardiovascular disease morbidity and mortality. However, little is known about the association of echocardiographic LV hypertrophy with sudden death. Methods. We examined the relations of LV mass and hypertrophy to the incidence of sudden death in 3,661 subjects enrolled in the Framingham Heart Study who were >40 years of age. The baseline examination was performed from 1979 to 1983 and LV hypertrophy was defined as LV mass (adjusted for height) >143 g/m in men and >102 g/m in women. During up to 14 years of follow-up there were 60 sudden deaths. Cox models examined the relations of LV mass and LV hypertrophy to sudden death risk after adjusting for known risk factors. Results. The prevalence of LV hypertrophy was 21.5%. The risk factor–adjusted hazard ratio (HR) for sudden death was 1.45 (95% confidence interval [CI] 1.10 to 1.92, p = 0.008) for each 50-g/m increment in LV mass. For LV hypertrophy, the risk factor–adjusted HR for sudden death was 2.16 (95% CI 1.22 to 3.81, p = 0.008). After excluding the first 4 years of follow-up, both increased LV mass and LV hypertrophy conferred long-term risk of sudden death (HR 1.53, 95% CI 1.01 to 2.28, p and HR 3.28, 95% CI 1.58 to 6.83, p , respectively). Conclusions. Increased LV mass and hypertrophy are associated with increased risk for sudden death after accounting for known risk factors. (J Am Coll Cardiol 1998;32:1454 –9)

QRS duration predicts sudden cardiac death in hypertensive patients undergoing intensive medical therapy: the LIFE study QRS > 110 ms QRS < 88 ms Cumulative incidence of sudden cardiac death, adjusting for competing risk of death from other causes, in relation to quartiles of baseline QRS duration. QRSd, QRS duration. QRS duration predicts sudden cardiac death in hypertensive patients undergoing intensive medical therapy: the LIFE study Eur Heart J Dec;30(23): Abstract AIMS: To determine whether QRS duration predicts sudden cardiac death (SCD) in patients with left ventricular hypertrophy and treated hypertension. METHODS AND RESULTS: Over 4.8 +/- 0.9 years follow-up of 9193 hypertensive patients with electrocardiographic evidence of LVH who were treated with atenolol- or losartan-based regimens, 178 patients (1.9%) suffered SCD. In multivariable analysis including randomized treatment, changing blood pressure over time, and baseline differences between patients with and without SCD, QRS duration was independently predictive of SCD (HR per 10 ms increase = 1.22, P < 0.001). Baseline QRS duration remained a significant predictor of SCD even after controlling for the presence or absence of left bundle branch block (HR = 1.17, P = 0.001) and for changes in ECG LVH severity over the course of the study (HR = 1.16, P = 0.017). CONCLUSION: In the setting of aggressive antihypertensive therapy, prolonged QRS duration identifies hypertensive patients at higher risk for SCD, even after controlling for left bundle branch block, other known risk factors for SCD, and changes in blood pressure and severity of left ventricular hypertrophy. Cumulative incidence of sudden cardiac death, adjusting for competing risk of death from other causes, in relation to quartiles of baseline QRS duration. .Eur Heart J 2009;30:

LBBB and CV morbidity and mortality in hypertensive patients with LVH: the LIFE study. J Hypertens Jun;26(6): HTA con HVI 564 pts con BCRI BCRI: independientemente asociado a: Muerte CV: HR= (95% IC , P < 0.05) MS: HR= (95% IC , P < 0.001) J Hypertens Jun;26(6): Left bundle branch block and cardiovascular morbidity and mortality in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension study. Li Z, Dahlöf B, Okin PM, Kjeldsen SE, Wachtell K, Ibsen H, Nieminen MS, Jern S, Devereux RB. Source Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA. Abstract BACKGROUND: Whether left bundle branch block is associated with cardiovascular events in hypertension with electrocardiographic left ventricular hypertrophy is unknown. METHODS: Hypertensive patients with electrocardiographic-left ventricular hypertrophy were randomized to losartan-based or atenolol-based treatment and followed for 4.8 years in the losartan intervention for endpoint reduction in hypertension study. Cox regression models controlling for significant covariates assessed the association of left bundle branch block with cardiovascular events. RESULTS: At baseline, 564 patients had left bundle branch block and 8567 patients did not. Left bundle branch block was associated with higher heart rate, electrocardiographic-left ventricular hypertrophy, and prior cardiovascular disease (all P < 0.005). In univariate Cox regression analysis, left bundle branch block was not associated with the composite endpoint, stroke, or myocardial infarction (all P > 0.05), and was associated with cardiovascular (8.3 versus 4.5%, P < 0.001) and all-cause mortality (12.1 versus 8.6%, P < 0.005). After adjusting for significant covariates Cox regression analyses showed that left bundle branch block was independently associated with 1.6-fold more cardiovascular death (95% confidence interval , P < 0.05), 1.7 fold more hospitalization for heart failure (95% confidence interval , P < 0.01), 3.5 fold more cardiovascular death within 1 h (95% confidence interval , P < 0.001), and 3.4 fold more cardiovascular death within 24 h (95% confidence interval , P < 0.001). CONCLUSION: In hypertension with electrocardiographic-left ventricular hypertrophy, left bundle branch block identifies patients at increased risk of cardiovascular mortality, sudden cardiovascular death, and heart failure.

Medición de dispersión de QTc, Arritmias V e HVI
QT Dispersion and Left Ventricular Hypertrophy in Elderly Hypertensive and Normotensive Patients ANGIOLOGY : 60 HTA 48 controles Medición de dispersión de QTc, Arritmias V e HVI HTA + HVI (P = .006) + dispersión del QTc (P = .004) Los HVI + incidencia de Lown's score (P < .001), + dispersión del QTc (P < .001). QT Dispersion and Left Ventricular Hypertrophy in Elderly Hypertensive and Normotensive Patients ANGIOLOGY October/November : Inhomogeneity of ventricular repolarization as detected by QT dispersion may be a potential leading mechanism of sudden death in hypertensive and normotensive (age related) left ventricular hypertrophy. Aim of this study was to investigate QT dispersion, ventricular arrhythmias, and left ventricular mass index in elderly hypertensive and normotensive patients. Study population consisted of 60 consecutive patients (sex: 34 men/26 women; age: 63 ± 11 years) with essential arterial hypertension and 48 age and sex-matched control subjects (24 men/24 women; 64 ± 16 years). Measurements included QTc dispersion, ventricular arrhythmias, and left ventricular hypertrophy. Hypertensive patients had greater left ventricular mass index (P = .006) and higher QTc dispersion (P = .004) than controls. Left ventricular hypertrophy was diagnosed in 57 (31 men/26 women) of all subjects. These patients had higher blood pressure (P < .05), Lown's score (P < .001), and QTc dispersion (P < .001). QTc dispersion and Lown's score were independent predictors of left ventricular mass index (P < .001). Conclusively, QTc dispersion is a strong indicator of left ventricular mass index and might be used in risk stratification of hypertensive and normotensive elderly patients.

CLINICAL BIOMARKERS OF ARRHYTHMIC RISK
The association between QT dispersion and left ventricular mass in hypertensive patients has been demonstrated [97], as well as the strong correlation with the prevalence of complex ventricular arrhythmias [98]. Several studies showed a significant prognostic value of QTc dispersion in hypertensive subjects [99,100], which has been nevertheless challenged by other studies [101]. Current Pharmaceutical Design, 2011, 17, /11 $ © 2011 Bentham Science Publishers Markers of Arrhythmogenic Risk in Hypertensive Subjects Andrea Barison1,2, Giuseppe Vergaro1, Luigi Emilio Pastormerlo1, Lorenzo Ghiadoni3, Michele Emdin1 and Claudio Passino1,2,* 1Fondazione “G. Monasterio” CNR - Regione Toscana, Pisa, Italy, 2Scuola Superiore Sant’Anna, Pisa, Italy, 3Department of Internal Medicine, University of Pisa, Pisa, Italy Abstract: Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias.

RESONANCIA MAGNETICA CARDIACA
Marcadora de: Hipertrofia Dilatación, disfunción sistólica Fibrosis [129] Puntmann VO, Jahnke C, Gebker R, et al. Usefulness of Magnetic Resonance Imaging to Distinguish Hypertensive and Hypertrophic Cardiomyopathy. Am J Cardiol 2010; 106: [130] Rudolph A, Abdel-Aty H, Bohl S, et al. Noninvasive detection of fibrosis applying contrast-enhanced cardiac magnetic resonance in different forms of left ventricular hypertrophy relation to remodeling. J Am Coll Cardiol 2009; 53: [131] Andersen K, Hennersdorf M, Cohnena M, Blondin D, Modder U, Poll LW. Myocardial delayed contrast enhancement in patients with arterial hypertension: Initial results of cardiac MRI. Eur J Rad 2009; 71: 75-81 Current Pharmaceutical Design, 2011, 17, /11 $ © 2011 Bentham Science Publishers Markers of Arrhythmogenic Risk in Hypertensive Subjects Andrea Barison1,2, Giuseppe Vergaro1, Luigi Emilio Pastormerlo1, Lorenzo Ghiadoni3, Michele Emdin1 and Claudio Passino1,2,* 1Fondazione “G. Monasterio” CNR - Regione Toscana, Pisa, Italy, 2Scuola Superiore Sant’Anna, Pisa, Italy, 3Department of Internal Medicine, University of Pisa, Pisa, Italy Abstract: Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias.

Relation to Remodeling
Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy: Relation to Remodeling (Left) Incidence of late gadolinium enhancement (LGE) in patients with aortic stenosis (AS), arterial hypertension (AH), and hypertrophic cardiomyopathy (HCM). (Middle) Incidence of LGE within each segment (percentage) of all patients, including those with and without LGE. In HCM the late enhancement was predominantly anteroseptal and inferoseptal. In AS and AH no specific pattern of fibrosis could be identified. (Right) Representative short-axis slice images showing location of LGE (red arrows). Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy: Remodeling J Am Coll Cardiol. 2009;53(3): Objectives We aimed to evaluate the incidence and patterns of late gadolinium enhancement (LGE) in different forms of left ventricular hypertrophy (LVH) and to determine their relation to severity of left ventricular (LV) remodeling. Background Left ventricular hypertrophy is an independent predictor of cardiac mortality. The relationship between LVH and myocardial fibrosis as defined by LGE cardiovascular magnetic resonance (CMR) is not well understood. Methods A total of 440 patients with aortic stenosis (AS), arterial hypertension (AH), or hypertrophic cardiomyopathy (HCM) fulfilling echo criteria of LVH underwent CMR with assessment of LV size, weight, function, and LGE. Patients with increased left ventricular mass index (LVMI) resulting in global LVH in CMR were included in the study. Results Criteria were fulfilled by 83 patients (56 men, age 57 ± 14 years; AS, n = 21; AH, n = 26; HCM, n = 36). Late gadolinium enhancement was present in all forms of LVH (AS: 62%, AH: 50%; HCM: 72%, p = NS) and was correlated with LVMI (r = 0.237, p = 0.045). There was no significant relationship between morphological obstruction and LGE. The AS subjects with LGE showed higher LV end-diastolic volumes than those without (1.0 ± 0.2 ml/cm vs. 0.8 ± 0.2 ml/cm, p < 0.015). Typical patterns of LGE were observed in HCM but not in AS and AH. Conclusions Fibrosis as detected by CMR is a frequent feature of LVH, regardless of its cause, and depends on the severity of LV remodeling. As LGE emerges as a useful tool for risk stratification also in nonischemic heart diseases, our findings have the potential to individualize treatment strategies. J Am Coll Cardiol. 2009;53(3):

HTA, con HVI + AV + MS

Es la arritmia per sé un mecanismo importante en la MS
Es la arritmia per sé un mecanismo importante en la MS? La prevención, o la regresión de HVI en HTA: disminuye la incidencia de MS?

Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death . The LIFE Study Circulation 2007;116:700–705 9193 pts 55 to 80 a, HTA esencial HVI por ECG Seguimiento medio = a MS = 190 pts (2%) Arrhythmia/Electrophysiology Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death The LIFE Study Background— Sudden cardiac death (SCD) occurs more often in patients with ECG left ventricular (LV) hypertrophy. However, whether LV hypertrophy regression is associated with a reduced risk of SCD remains unclear. Methods and Results— The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study included 9193 patients 55 to 80 years of age with essential hypertension and ECG LV hypertrophy by gender-adjusted Cornell product (CP) (RaVL+SV3 [+6 mm in women]) · QRS duration>2440 mm · ms) and/or Sokolow-Lyon voltage (SLV) (SV1+RV5/6>38 mm). During follow-up (mean, 4.8 years), 190 patients (2%) experienced SCD. In time-dependent Cox analyses, absence of in-treatment LV hypertrophy was associated with a decreased risk of SCD: every 1-SD-lower in-treatment CP (1050 mm · ms) was associated with a 28% lower risk of SCD (hazard ratio [HR], 0.72; 95% CI, 0.66 to 0.79) and 1-SD-lower SLV (10.5 mm) with a 26% lower risk (HR, 0.74; 95% CI, 0.65 to 0.84). After adjustment for time-varying systolic and diastolic blood pressures, treatment allocation, age, gender, baseline Framingham risk score, ECG strain, heart rate, urine albumin/creatinine ratio, smoking, diabetes, congestive heart failure, coronary heart disease, atrial fibrillation, and occurrence of myocardial infarction, atrial fibrillation, heart failure, and noncardiovascular death, both in-treatment CP and SLV remained predictive of SCD: each 1-SD-lower CP was associated with a 19% lower risk of SCD (HR, 0.81; 95% CI, 0.73 to 0.90) and 1-SD-lower SLV with an 18% lower risk (HR, 0.82; 95% CI, 0.70 to 0.98). Absence of in-treatment LV hypertrophy by both SLV and CP was associated with a 30% lower risk of SCD (HR, 0.70; 95% CI, 0.54 to 0.92). Conclusions— Absence of in-treatment ECG LV hypertrophy is associated with reduced risk of SCD independently of treatment modality, blood pressure reduction, prevalent coronary heart disease, and other cardiovascular risk factors in hypertensive patients with LV hypertrophy.

Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death The LIFE Study Circulation 2007;116:700–705 Figure 1. Kaplan-Meier curves for occurrence of SCD in losartan- and atenolol-treated hypertensive patients with LV hypertrophy. Figure 1. Kaplan-Meier curves for occurrence of SCD in losartan- and atenolol-treated hypertensive patients with LV hypertrophy. Circulation 2007;116:

Regression of Electrocardiographic Left Ventricular Hypertrophy During Antihypertensive Therapy and Reduction in Sudden Cardiac Death The LIFE Study Circulation 2007;116:700–705 Figure 2. Modified Kaplan-Meier curves showing the rate of SCD according to time-varying presence or absence of ECG LV hypertrophy according to gender-specific Cornell voltage-duration product partitioned at 2000, 2500, and 3000 mm · ms. Patient group assignment is adjusted at the time of each ECG on the basis of the value of the Cornell product at each time (n=number of patients at risk in each group at study baseline and every year of the study). Figure 2. Modified Kaplan-Meier curves showing the rate of SCD according to time-varying presence or absence of ECG LV hypertrophy according to gender-specific Cornell voltage-duration product partitioned at 2000, 2500, and 3000 mm · ms. Circulation 2007;116:

HTA Y FIBRILACION AURICULAR

SITUACIONES CLINICAS ASOCIADAS A FIBRILACION AURICULAR
Miocardiopatías Valvulopatía Mitral Hipertensión Arterial Diabetes Hipertiroidismo Cirugía Cardíaca Cardiopatías Congénitas Pericarditis Enfermedad Pulmonar Solitaria Neurogénicas Inducidas por Taquicardia

38 años de seguimiento en el Estudio Framingham :
“Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates” 38 años de seguimiento en el Estudio Framingham : HTA: aumento de riesgo de FA 1,5 en hombres, 1,4 en mujeres Predictores ecocardiográficos para FA: Agrandamiento de AI (39% de incremento de riesgo por cada 5-mm ) Espesor de pared VI (28% por 4-mm incremento). Fracción de Acortamiento de VI (34% por 5% decremento) Abstract Atrial fibrillation (AF) is the most common of the serious cardiac rhythm disturbances and is responsible for substantial morbidity and mortality in the general population. Its prevalence doubles with each advancing decade of age, from 0.5% at age 50–59 years to almost 9% at age 80–89 years. It is also becoming more prevalent, increasing in men aged 65–84 years from 3.2% in 1968–1970 to 9.1% in 1987–1989. This statistically significant increase in men was not explained by an increase in age, valve disease, or myocardial infarctions in the cohort. The incidence of new onset of AF also doubled with each decade of age, independent of the increasing prevalence of known predisposing conditions. Based on 38-year follow-up data from the Framingham Study, men had a 1.5-fold greater risk of developing AF than women after adjustment for age and predisposing conditions. Of the cardiovascular risk factors, only hypertension and diabetes were significant independent predictors of AF, adjusting for age and other predisposing conditions. Cigarette smoking was a significant risk factor in women adjusting only for age (OR = 1.4), but was just short of significance on adjustment for other risk factors. Neither obesity nor alcohol intake was associated with AF incidence in either sex. For men and women, respectively, diabetes conferred a 1.4- and 1.6-fold risk, and hypertension a 1.5- and 1.4-fold risk, after adjusting for other associated conditions. Because of its high prevalence in the population, hypertension was responsible for more AF in the population (14%) than any other risk factor. Intrinsic overt cardiac conditions imposed a substantially higher risk. Adjusting for other relevant conditions, heart failure was associated with a 4.5- and 5.9-fold risk, and valvular heart disease a 1.8- and 3.4-fold risk for AF in men and women, respectively. Myocardial infarction significantly increased the risk factor-adjusted likelihood of AF by 40% in men only. Echocardiographic predictors of nonrheumatic AF include left atrial enlargement (39% increase in risk per 5-mm increment), left ventricular fractional shortening (34% per 5% decrement), and left ventricular wall thickness (28% per 4-mm increment). These echocardiographic features offer prognostic information for AF beyond the traditional clinical risk factors. Electrocardiographic left ventricular hypertrophy increased risk of AF 3–4-fold after adjusting only for age, but this risk ratio is decreased to 1.4 after adjustment for the other associated conditions. The chief hazard of AF is stroke, the risk of which is increased 4–5-fold. Because of its high prevalence in advanced age, AF assumes great importance as a risk factor for stroke and by the ninth decade becomes a dominant factor. The attributable risk for stroke associated with AF increases steeply from 1.5% at age 50–59 years to 23.5% at age 80–89 years. AF is associated with a doubling of mortality in both sexes, which is decreased to 1.5–1.9-fold after adjusting for associated cardiovascular conditions. Decreased survival associated with AF occurs across a wide range of ages. American Journal of Cardiology, 1998;82: 2N

Presión de Pulso y riesgo de aparición de FA
Framingham Heart Study: 5331 => 35 años y libres de FA inicialmente Incidencia acumulativa de FA a 20 años: 5.6% para una PP < 40 mm Hg 23.3% para una PP > 61 mm Hg Figure. Incidence of Atrial Fibrillation According to Quartiles of Pulse Pressure Estimates of cumulative incidence of atrial fibrillation according to quartile of pulse pressure. Cut points denoting approximate quartiles of pulse pressure were at 40, 49, and 61 mm Hg. Estimates are adjusted for age, sex, and competing risk of mortality. We hypothesized that the observed relation between pulse pressure and risk for developing AF may be attributable in part to the effects of abnormal arterial stiffness on pulsatile load and left ventricular structure and function, leading to abnormal left atrial structure and function. To test this hypothesis, we next added baseline echocardiographic left ventricular fractional shortening, left ventricular mass, and left atrial diameter to model 3 of Table 2, which included time-dependent clinical variables, pulse pressure, and mean arterial pressure. Left ventricular fractional shortening and left ventricular mass were significantly related to incident AF in these models. Pulse pressure remained a significant predictor in this model (HR, 1.23; 95% CI, ; P = .001). In a secondary analysis, we excluded people with imputed echocardiographic data, which reduced the number of AF events from 698 to 464. The pulse pressure effect was comparable in this model, although the P value was borderline because of reduced power (HR, 1.17; 95% CI, ; P = .05). Incidence of Atrial Fibrillation According to Quartiles of Pulse Pressure Estimates of cumulative incidence of atrial fibrillation according to quartile of pulse pressure. Mitchell, G. F. et al. JAMA 2007;297:

SOBREVIDA LIBRE DE FIBRILACION AURICULAR SEGUN FUNCION DIASTOLICA
Tsang, T. S. M. et al. J Am Coll Cardiol 2002;40: Age-adjusted cumulative survival without nonvalvular atrial fibrillation (NVAF) by diastolic function profile Riesgo de FA a 5 años, ajustado a edad: 1% 12% 14% 21% . Olmsted County, Minnesota, población > 65 años SOBREVIDA LIBRE DE FIBRILACION AURICULAR SEGUN FUNCION DIASTOLICA Figure 2 Age-adjusted cumulative survival without nonvalvular atrial fibrillation (NVAF) by diastolic function profile. Left atrial size is certainly easy to assess. With the advent of hand-carried ultrasound, it can be a bedside or point of care measure, possibly routinely obtainable as part of a comprehensive physical examination. Even more important, the Tsang et al. (2) data suggest that the hypothesis that LA size represents the integration of LV diastolic performance over time is clinically valid. Left atrial volume thereby provides a long-term view of whether or not the patient has the "disease" of diastolic dysfunction, regardless of whatever loading conditions are present at the time of the examination.

HIPERTENSION ARTERIAL
Vaziri, S. M. et al. Hypertension 1995;25: Bar graphs show age-adjusted prevalence of left atrial enlargement according to 8-year average systolic pressure in men and women Influencia de la Presión Arterial sobre el tamaño de la Auricula Izquierda The Framingham Heart Study HIPERTENSION ARTERIAL Y DILATACION AURICULAR Figure 1. Bar graphs show age-adjusted prevalence of left atrial enlargement according to 8-year average systolic pressure in men and women. Left atrial enlargement is defined as left atrial size 43 mm in men and 38 mm in women.

Influencia de la Presión Arterial sobre el tamaño de la Auricula Izquierda The Framingham Heart Study Figure 2. Bar graphs show age-adjusted prevalence of left atrial enlargement according to 8-year average pulse pressure in men and women. Left atrial enlargement is defined as left atrial size 43 mm in men and 38 mm in women. Bar graphs show age-adjusted prevalence of left atrial enlargement according to 8-year average pulse pressure in men and women Vaziri, S. M. et al. Hypertension 1995;25:

VOLUMEN DE AURICULA IZQUIERDA:
VALOR PRONOSTICO Figure 2 Age-adjusted cumulative survival without nonvalvular atrial fibrillation (NVAF) by diastolic function profile. Left atrial size is certainly easy to assess. With the advent of hand-carried ultrasound, it can be a bedside or point of care measure, possibly routinely obtainable as part of a comprehensive physical examination. Even more important, the Tsang et al. (2) data suggest that the hypothesis that LA size represents the integration of LV diastolic performance over time is clinically valid. Left atrial volume thereby provides a long-term view of whether or not the patient has the "disease" of diastolic dysfunction, regardless of whatever loading conditions are present at the time of the examination.

SOBREVIDA LIBRE DE FIBRILACION AURICULAR
SEGUN VOLUMEN DE AURICULA IZQUIERDA Olmsted County, Minnesota, población > 65 años Figure 1 Age-adjusted cumulative survival without nonvalvular atrial fibrillation (NVAF) by left atrial volume indexed to body surface area (LAVI). Age-adjusted cumulative survival without nonvalvular atrial fibrillation (NVAF) by left atrial volume indexed to body surface area (LAVI) Tsang, T. S. M. et al. J Am Coll Cardiol 2002;40:

Remodelamiento eléctrico- estructural
Genética Edad Factores adquiridos: Taquicardia Anormalidades en Presión /Volúmen Fibrosis Inflamación Isquemia S.R-A-A Aurículas con Remodelamiento eléctrico- estructural Moduladores SNA Hormonas Medio interno Disparadores F.A. Paroxística Permanente - Crónica Persistente

“Canales activados por estiramiento”
Bode, F. et al. Circulation 2000;101: Effect of atrial pressure on AF inducibility and AF duration in isolated rabbit heart during baseline Spontaneous AF after pressure increase from 12.5 to 15 cm H2O. Premature depolarizations and runs of nonsustained AF (*) evolved “Canales activados por estiramiento” Incrementan vulnerabilidad para FA Figure 1. Effect of atrial pressure on AF inducibility and AF duration in isolated rabbit heart during baseline. Bipolar electrogram recorded from right atrium. At low intra-atrial pressure (P) of 2.5 cm H2O, no AF response evolved after cessation of burst pacing (). With a stepwise increase in P, burst pacing induced AF episodes of progressively longer duration. At 12.5 cm H2O, sustained AF was evoked. Figure 4. Spontaneous AF after pressure increase from 12.5 to 15 cm H2O. Premature depolarizations () and runs of nonsustained AF (*) evolved.

Corazones aislados de conejos Sistema de electrodos múltiples en AD
Effects of Acute Atrial Dilation on Heterogeneity in Conduction in the Isolated Rabbit Heart S C.M. EIJSBOUTS, M A. ALLESSIE Incremento agudo de la presión intra-atrial Activación de los canales activados por estiramiento Desacoplamiento de las uniones gap Deterioro de conducción, líneas de bloqueo Figure 3. High-density maps of the free wall of the right atrium during regular pacing (interval 240 msec) from four different directions (A, B, C, and D) at an atrial pressure of 2 and 14 cm H2O. Activation times are given in milliseconds and isochrones are drawn at 3-msec intervals. Arrows indicate the main direction of propagation. The total conduction time of the mapped tissue is indicated by the encircled black numbers. The sites of recording of the electrograms shown at the bottom are labeled in map A. During dilation, the directional differences were larger and conduction was less uniform due to an increase in local conduction delays (crowding of isochrones). The electrograms decreased in amplitude and became more fractionated. Corazones aislados de conejos Sistema de electrodos múltiples en AD Estimulación desde 4 puntos diferentes a 240 y 125 msegs. Incremento agudo de la presión intra-atrial Conducción se deteriora con incrementos de la presión, provoca líneas de bloqueo Desacoplamiento de las uniones gap Activación de los canales activados por estiramiento El aumento en la heterogeneidad espacial en la conducción también estuvo relacionada a las propiedades anisotrópicas de la pared atrial J Cardiovasc Electrophysiol,2003;14:269

Inter-relaciones entre estiramiento, cardiomiocitos y fibroblastos
Cellular mediators. Fibrosis results when circulating and locally synthesized profibrotic factors act on resident cardiac cells to increase collagen production without offsetting increases in collagen degradation. Cardiomyocytes account for approximately 45% of the atrial myocardium by volume, compared with approximately 76% in the ventricles (68,69). Nonmyocytes are thought to compose approximately 70% of cardiac cells by number (70): atrial–ventricular differences in the composition of this heterogeneous population of cells may contribute to the greater atrial ECM volume compared with ventricles in normal hearts (68,69), which becomes exaggerated with remodeling (9). There is a complex interplay among these cell types, the most numerous of which is the cardiac fibroblast. The fibroblast was traditionally thought to be a passive bystander in the myocardium, but is now recognized to participate actively in shaping and responding to the cardiac milieu (71). Figure 3 is a schematic representation of cardiomyocyte–fibroblast crosstalk in the promotion of atrial fibrosis. Exposure to AngII (72) or TGF-β1 (73) dramatically influences cardiac fibroblast function, upregulating ECM protein synthesis and secretion. Both AngII production and AT1 receptor expression are increased during remodeling in fibroblasts in vivo (74). Increases in AngII and activated TGF-β1 concentrations reciprocally enhance each other’s production (56,75), and induce expression of additional profibrotic molecules in fibroblasts (76,77), creating positive feedback cycles for fibrosis. Mechanical stretch induces collagen synthesis (78), along with increased AngII and TGF-β1 expression in cardiac fibroblasts (79), and thus chronic atrial dilation may contribute to structural remodeling and the domestication of AF (80). Fibroblast stretch-sensing mechanisms show exquisite sensitivity, with different types of deformation causing differential ECM expression profiles (81). In addition to profibrotic actions, mechanical stretch of fibroblasts can directly modulate myocyte electrical activity, a potentially proarrhythmic mechanism called mechanoelectric feedback (82). Although cardiomyocytes probably do not directly synthesize collagen (83), they can importantly influence structural remodeling through interactions with neighboring fibroblasts. Mechanical stretch induces cardiomyocyte mitogen-activated protein kinase signaling through direct activation of AT1 receptors (84). Angiotensin II is produced by stretched cardiomyocytes (85), with direct fibroblast-activating consequences. Furthermore, AngII acts as a paracrine/autocrine hypertrophic signal, and eventual myocyte failure and death further promotes fibroblast chemotaxis. Rapid cardiomyocyte activation seems to cause AngII upregulation (52,86) and tachypaced atrial cardiomyocytes secrete factors that cause differentiation to a secretory phenotype in cardiac fibroblasts (87). In coculture experiments, cardiomyocytes potentiate AngII-stimulated collagen synthesis in fibroblasts (88,89). The potential importance of cardiomyocyte–fibroblast interactions in fibrillating atria has recently been emphasized based on observations on atrial myocytes from AF patients (90). Burstein, B. et al. J Am Coll Cardiol 2008;51:

HTA S.R-A-A Presión Dilatación Hipertrofia Fibrosis Inflamación
Atrial tissue from patients with AF shows significant abnormalities. Most of the described structural changes are related to altered signal transduction at the cellular level. Activation of intracellular MAP kinases by various stimuli (heptahelical receptor agonists, growth factors, etc.) seems to play an especially important role. Activated MAP kinases can contribute to hypertrophy of atrial myocytes, apoptosis and alterations of interstitial matrix composition in patients with AF. In addition to MAP kinase-dependent effects, loss of cell–matrix interactions by increased ADAM expression is associated with atrial dilation. Activation of PKC-dependent pathways can influence atrial potassium and calcium currents. Furthermore, stimulation of signaling pathways and their complex interactions may help to explain why electrophysiological and structural components of ‘atrial remodeling’ are at least partially dissociable. Paroxysmal episodes of AF, which do not induce long-lasting electrophysiological abnormalities, may cause prolonged alterations in atrial signal transduction and gene expression. Accumulation of such changes may contribute to the conversion of an ‘electrical abnormality’ into a ‘structural atrial disease’. In contrast, in the presence of cardiovascular diseases like hypertension or heart failure, AF appears as a consequence rather than a primary cause of altered signal transduction. However, more experimental evidence is needed to clarify these important issues. Further elucidation of atrial signal transduction systems and their regulation will contribute to a better understanding of the pathophysiology of AF and, in addition, may offer novel therapeutic and prophylactic approaches in the future. Alteración en refractariedad conducción FIBRILACION AURICULAR

BLOQUEO DEL SISTEMA RENINA-ANGIOTENSINA FIBRILACION AURICULAR
Y FIBRILACION AURICULAR

The Losartan Intervention For Endpoint reduction in hypertension
(LIFE) 881 pts, HTA / HVI “Nueva FA”= 290 pts Figure 2 Kaplan-Meier curves illustrating new-onset electrocardiogram-verified atrial fibrillation during follow-up. CI = confidence interval; HR = hazard ratio. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol The Losartan Intervention For End point reduction in hypertension (LIFE) study J Am Coll Cardiol 2005;45: Kaplan-Meier curves illustrating new-onset electrocardiogram-verified atrial fibrillation during follow-up J Am Coll Cardiol 2005;45:

(LIFE) 881 pts, HTA / HVI 881 pts HTA, HVI Figure 1. Mean left atrial diameter at baseline and at annual echocardiograms in patients randomly assigned to atenolol- (—) or losartan- (---) based antihypertensive treatment (*P<0.01 vs baseline within group). The influence of left atrial size on cardiovascular events during antihypertensive treatment has not been reported previously from a long-term, prospective, randomized hypertension treatment trial. We recorded left atrial diameter by annual echocardiography and cardiovascular events in 881 hypertensive patients (41% women) with electrocardiographic left ventricular hypertrophy aged 55 to 80 (mean: 66) years during a mean of 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Study. During follow-up, a total of 88 primary end points (combined cardiovascular death, myocardial infarction, or stroke) occurred. In Cox regression, baseline left atrial diameter/height predicted incidence of cardiovascular events (hazard ratio: 1.98 per cm/m [95% CI: 1.02 to 3.83 per cm/m]; P=0.042) adjusted for significant effects of Framingham risk score and history of atrial fibrillation. Greater left atrial diameter reduction during follow-up was associated with greater reduction in left ventricular hypertrophy, absence of new-onset atrial fibrillation or mitral regurgitation during follow-up, and losartan-based treatment (B=–0.13±0.03 cm/m; P<0.001) in multiple linear regression, adjusting for baseline left atrial diameter/height. However, in time-varying Cox regression analysis, left atrial diameter reduction was not independent of left ventricular hypertrophy regression in predicting cardiovascular events during follow-up. In conclusion, left atrial diameter/height predicts risk of cardiovascular events independent of other clinical risk factors in hypertensive patients with left ventricular hypertrophy and may be useful in pretreatment clinical assessment of cardiovascular risk in these patients. Mean left atrial diameter at baseline and at annual echocardiograms in patients randomly assigned to atenolol- (--) or losartan- (---) based antihypertensive treatment (*P<0.01 vs baseline within group) Gerdts, E. et al. Hypertension 2007;49:

JAMA 2006;296: Figure. Rate of New-Onset Atrial Fibrillation Rate is according to time-varying presence or absence of electrocardiographic left ventricular hypertrophy according to sex-specific Cornell voltage-duration product criteria partitioned at 2440 mm × msec. The Losartan Intervention For Endpoint reduction in hypertension (LIFE) 831 pts, HTA. HVI Pts con regresión o no presencia = nueva FA en 14,9%o pt-año Pts con persistencia o desarrollo = nueva FA en 19,0%o pt-año Figure. Rate of New-Onset Atrial Fibrillation Rate is according to time-varying presence or absence of electrocardiographic left ventricular hypertrophy according to sex-specific Cornell voltage-duration product criteria partitioned at 2440 mm × msec. Patient group assignment is adjusted at the time of each electrocardiogram based on the value of Cornell product at each time point. Regression of Electrocardiographic Left Ventricular Hypertrophy and Decreased Incidence of New-Onset Atrial Fibrillation in Patients With Hypertension Peter M. Okin, MD JAMA. 2006;296(10): Abstract Context Atrial fibrillation (AF) is associated with increased risk of mortality and cardiovascular events, particularly stroke, making prevention of new-onset AF a clinical priority. Although the presence and severity of electrocardiographic left ventricular hypertrophy (LVH) appear to predict development of AF, whether regression of electrocardiographic LVH is associated with a decreased incidence of AF is unclear. Objective To test the hypothesis that in-treatment regression or continued absence of electrocardiographic LVH during antihypertensive therapy is associated with a decreased incidence of AF, independent of blood pressure and treatment modality. Design, Setting, and Participants Double-blind, randomized, parallel-group study conducted in among 8831 men and women with hypertension, aged years (median, 67 years), with electrocardiographic LVH by Cornell voltage-duration product or Sokolow-Lyon voltage, with no history of AF, without AF on the baseline electrocardiogram, and enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Interventions Losartan- or atenolol-based treatment regimens, with follow-up assessments at 6 months and then yearly until death or study end. Main Outcome Measure New-onset AF in relation to electrocardiographic LVH determined at baseline and subsequently. Electrocardiographic LVH was measured using sex-adjusted Cornell product criteria ({RaVL + SV3 [+ 6 mm in women]} × QRS duration). Results After a mean (SD) follow-up of 4.7 (1.1) years, new-onset AF occurred in 290 patients with in-treatment regression or continued absence of Cornell product LVH for a rate of 14.9 per 1000 patient-years and in 411 patients with in-treatment persistence or development of LVH by Cornell product criteria for a rate of 19.0 per 1000 patient-years. In time-dependent Cox analyses adjusted for treatment effects, baseline differences in risk factors for AF, baseline and in-treatment blood pressure, and baseline severity of electrocardiographic LVH, lower in-treatment Cornell product LVH treated as a time-varying covariate was associated with a 12.4% lower rate of new-onset AF (adjusted hazard ratio [HR], 0.88; 95% CI, ; P = .007) for every 1050 mm × msec (per 1-SD) lower Cornell product, with persistence of the benefit of losartan vs atenolol therapy on developing AF (HR, 0.83; 95% CI, ; P = .01). Conclusions Lower Cornell product electrocardiographic LVH during antihypertensive therapy is associated with a lower likelihood of new-onset AF, independent of blood pressure lowering and treatment modality in essential hypertension. These findings suggest that antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence

Prevention of Atrial Fibrillation by Renin-Angiotensin
Schneider, M. P. et al. J Am Coll Cardiol 2010;55: Prevention of Atrial Fibrillation by Renin-Angiotensin System Inhibition. A Meta-Analysis Figure 1 Effect of RAS Inhibition on Occurrence of AF Effect of angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) treatment on the occurrence of atrial fibrillation (AF) in primary prevention (hypertension, post-myocardial infarction [MI], and heart failure studies) and in secondary prevention (post-cardioversion and medical therapy studies). CAPPP = Captopril Prevention Project; CHARM = Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity; CI = confidence interval; GISSI-AF = Gruppo Italiano per lo Studio Della Sopravvivenza Nell'Infarto Miocardico–Atrial Fibrillation; GISSI-3 = Gruppo Italiano per lo Studio Della Sopravvivenza Nell'Infarto Miocardico–3; HOPE = Heart Outcomes Prevention Evaluation; LIFE = Losartan Intervention For Endpoint Reduction in Hypertension; OR = odds ratio; RAS = renin-angiotensin system; STOP-2 = Swedish Trial in Old Patients With Hypertension-2; TRACE = Trandolapril Cardiac Evaluation; TRANSCEND = Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease; Val-HeFT = Valsartan Heart Failure Trial; VALUE = Valsartan Antihypertensive Long-Term Use Evaluation. Primary prevention. Hypertension Six trials compared ACEIs or ARBs with other agents for the treatment of arterial hypertension. Overall, no significant reduction in the OR for AF was detectable (OR: 0.89; 95% CI: 0.75 to 1.05; p = 0.17). However, there was significant heterogeneity among trials (chi-square test, p = 0.003). CAPPP (Captopril Prevention Project) (26), STOP-2 (Swedish Trial in Old Patients With Hypertension-2) (17), the HOPE (Heart Outcomes Prevention Evaluation) study (27), and the recent TRANSCEND (Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease) (28) did not detect any effect of treatment with an ACEI or an ARB. In contrast, the LIFE (Losartan Intervention For Endpoint Reduction in Hypertension) (29) and the VALUE (Valsartan Antihypertensive Long-Term Use Evaluation) (30) trials, both testing the effect of ARBs, detected significant reductions in the rates of new-onset AF. In VALUE (30), hypertension was required as an inclusion criterion, and this study detected a modest but significant reduction in new-onset AF from 4.34% with amlodipine to 3.67% with valsartan. However, this was at odds with blood pressure lowering per se, as the blood pressure reduction was slightly greater in amlodipine-treated patients than in valsartan-treated patients, suggesting that mechanisms beyond blood pressure control may have contributed to the beneficial effects of valsartan. The largest reduction of new-onset AF was found in the LIFE study, from 5.28% in the atenolol group to 2.49% in the losartan group, which was associated with a reduced risk for cardiovascular morbidity and mortality, stroke, and hospitalization for heart failure for similar blood pressure reduction (37). The lower incidence of AF during treatment with losartan was associated with greater regression of left ventricular hypertrophy and greater reduction of left atrial size compared to treatment with atenolol (38,39). By Medical Therapy Four studies examined the effects of treatment with ACEIs or ARBs on the recurrence of AF in patients with paroxysmal AF. Overall, there was a significant reduction in the recurrence of AF with ACEI or ARB treatment (OR: 0.37; 95% CI: 0.27 to 0.49; p < 0.001). In contrast to the other subgroups, the 4 included studies were homogeneous (chi-square test, p = 0.49), and all 4 studies documented large and significant reductions in the risk for AF by RAS inhibition The 3 studies by Fogari et al. (18,52,53) focused on patients with arterial hypertension and used active comparator drugs. The first trial demonstrated that recurrence rates are lower with losartan and amiodarone than with amlodipine and amiodarone (52). The second compared the effects of valsartan, ramipril, and amlodipine without concurrent treatment with amiodarone (18). A lower recurrence rate of AF was found with both RAS inhibitors compared with amlodipine despite similar blood pressure lowering, again suggesting beneficial effects of RAS inhibition beyond blood pressure control. Interestingly, the beneficial effect was greater in patients receiving valsartan compared with ramipril, which was associated with more favorable effects on P-wave dispersion. The third study, in patients with hypertension and type 2 diabetes, demonstrated that valsartan or amlodipine is superior to atenolol or amlodipine, despite similar effects on peripheral blood pressure (53). Again, this might not be true for central blood pressure (15). J Am Coll Cardiol, 2010; 55:2299

Prevention of Atrial Fibrillation by Renin-Angiotensin
System Inhibition. A Meta-Analysis Fogari 1= 222 pts con HTA leve, FA previa: Losartan/Amiod vs Amlodipina/Amiod Fogari 2= 369 pts con HTA leve, FA previa: Ramipril o Valsartan vs Amlodipina Fogari 3= 296 pts con HTA leve, FA previa y diabetes: Valsartan/Amlodipina vs Atenolol/Amlod J Am Coll Cardiol, 2010; 55:2299 Figure 1 Effect of RAS Inhibition on Occurrence of AF Effect of angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) treatment on the occurrence of atrial fibrillation (AF) in primary prevention (hypertension, post-myocardial infarction [MI], and heart failure studies) and in secondary prevention (post-cardioversion and medical therapy studies). CAPPP = Captopril Prevention Project; CHARM = Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity; CI = confidence interval; GISSI-AF = Gruppo Italiano per lo Studio Della Sopravvivenza Nell'Infarto Miocardico–Atrial Fibrillation; GISSI-3 = Gruppo Italiano per lo Studio Della Sopravvivenza Nell'Infarto Miocardico–3; HOPE = Heart Outcomes Prevention Evaluation; LIFE = Losartan Intervention For Endpoint Reduction in Hypertension; OR = odds ratio; RAS = renin-angiotensin system; STOP-2 = Swedish Trial in Old Patients With Hypertension-2; TRACE = Trandolapril Cardiac Evaluation; TRANSCEND = Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease; Val-HeFT = Valsartan Heart Failure Trial; VALUE = Valsartan Antihypertensive Long-Term Use Evaluation. Primary prevention. Hypertension Six trials compared ACEIs or ARBs with other agents for the treatment of arterial hypertension. Overall, no significant reduction in the OR for AF was detectable (OR: 0.89; 95% CI: 0.75 to 1.05; p = 0.17). However, there was significant heterogeneity among trials (chi-square test, p = 0.003). CAPPP (Captopril Prevention Project) (26), STOP-2 (Swedish Trial in Old Patients With Hypertension-2) (17), the HOPE (Heart Outcomes Prevention Evaluation) study (27), and the recent TRANSCEND (Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease) (28) did not detect any effect of treatment with an ACEI or an ARB. In contrast, the LIFE (Losartan Intervention For Endpoint Reduction in Hypertension) (29) and the VALUE (Valsartan Antihypertensive Long-Term Use Evaluation) (30) trials, both testing the effect of ARBs, detected significant reductions in the rates of new-onset AF. In VALUE (30), hypertension was required as an inclusion criterion, and this study detected a modest but significant reduction in new-onset AF from 4.34% with amlodipine to 3.67% with valsartan. However, this was at odds with blood pressure lowering per se, as the blood pressure reduction was slightly greater in amlodipine-treated patients than in valsartan-treated patients, suggesting that mechanisms beyond blood pressure control may have contributed to the beneficial effects of valsartan. The largest reduction of new-onset AF was found in the LIFE study, from 5.28% in the atenolol group to 2.49% in the losartan group, which was associated with a reduced risk for cardiovascular morbidity and mortality, stroke, and hospitalization for heart failure for similar blood pressure reduction (37). The lower incidence of AF during treatment with losartan was associated with greater regression of left ventricular hypertrophy and greater reduction of left atrial size compared to treatment with atenolol (38,39). By Medical Therapy Four studies examined the effects of treatment with ACEIs or ARBs on the recurrence of AF in patients with paroxysmal AF. Overall, there was a significant reduction in the recurrence of AF with ACEI or ARB treatment (OR: 0.37; 95% CI: 0.27 to 0.49; p < 0.001). In contrast to the other subgroups, the 4 included studies were homogeneous (chi-square test, p = 0.49), and all 4 studies documented large and significant reductions in the risk for AF by RAS inhibition The 3 studies by Fogari et al. (18,52,53) focused on patients with arterial hypertension and used active comparator drugs. The first trial demonstrated that recurrence rates are lower with losartan and amiodarone than with amlodipine and amiodarone (52). The second compared the effects of valsartan, ramipril, and amlodipine without concurrent treatment with amiodarone (18). A lower recurrence rate of AF was found with both RAS inhibitors compared with amlodipine despite similar blood pressure lowering, again suggesting beneficial effects of RAS inhibition beyond blood pressure control. Interestingly, the beneficial effect was greater in patients receiving valsartan compared with ramipril, which was associated with more favorable effects on P-wave dispersion. The third study, in patients with hypertension and type 2 diabetes, demonstrated that valsartan or amlodipine is superior to atenolol or amlodipine, despite similar effects on peripheral blood pressure (53). Again, this might not be true for central blood pressure (15).

En HTA: La presencia de HVI y de Arritmia Ventricular
CONCLUSIONES HTA: factor de riesgo para arritmias SVs y Vs. En HTA: factores de riesgo / marcadores de Arritmias: Disfunción diastólica Agrandamiento de AI HVI Ensanchaniento del QRS BCRI Current Pharmaceutical Design, 2011, 17, /11 $ © 2011 Bentham Science Publishers Markers of Arrhythmogenic Risk in Hypertensive Subjects Andrea Barison1,2, Giuseppe Vergaro1, Luigi Emilio Pastormerlo1, Lorenzo Ghiadoni3, Michele Emdin1 and Claudio Passino1,2,* 1Fondazione “G. Monasterio” CNR - Regione Toscana, Pisa, Italy, 2Scuola Superiore Sant’Anna, Pisa, Italy, 3Department of Internal Medicine, University of Pisa, Pisa, Italy Abstract: Hypertension is increasingly considered a strong and independent risk factor for supraventricular and ventricular arrhythmias. The presence and complexity of both supraventricular and ventricular arrhythmias influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the foremost underlying risk factors for supraventricular and ventricular arrhythmias in hypertensive patients. In particular, the presence of hypertension is a risk for sudden death and this risk is higher in those with left ventricular hypertrophy. Moreover, arrhythmias in the hypertrophic heart are often facilitated and aggravated by electrolyte disturbances, sympatho-vagal unbalance, transient blood pressure peaks, and occurrence of myocardial ischaemia. Several noninvasive biohumoral, electrocardiographic and imaging parameters have been widely investigated to identify hypertensive patients at higher risk for the development of arrhythmias. These parameters include neurohormones, signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis, as well as echocardiographic and magnetic resonance indexes of atrial and ventricular shape and function. The aim of this review is to evaluate the relationship of high blood pressure with ventricular and supraventricular arrhythmias, to discuss the available biomarkers for arrhythmic risk assessment in hypertensive patients and the effects of a tailored tight blood pressure control on the occurrence of arrhythmias. En HTA: La presencia de HVI y de Arritmia Ventricular = + riesgo de Mort CV y MS

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