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Left ventricular hypertrophy and arrhythmia

Left ventricular hypertrophy and arrhythmia
Literature review current through: Jan 2024.
This topic last updated: May 09, 2022.

INTRODUCTION — Left ventricular hypertrophy (LVH) is a common finding in patients with cardiovascular disease (CVD) and CVD risk factors and is diagnosed either by electrocardiogram (ECG) or imaging (eg, echocardiography, cardiovascular computed tomography, cardiovascular magnetic resonance [CMR] imaging) [1]. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)

LVH has been associated with both ventricular and supraventricular arrhythmias [2]. Data, primarily from the Framingham Heart Study, have identified electrocardiographic LVH as a blood pressure-independent risk for sudden cardiac death (SCD) [3,4], acute myocardial infarction [5], and other cardiovascular morbidity and mortality [6]. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "Left ventricular hypertrophy: Clinical findings and ECG diagnosis", section on 'Prognosis'.)

This topic will review the association between LVH and arrhythmias (both ventricular and supraventricular) as well as sudden cardiac death.

DEFINITION AND ETIOLOGIES OF LVH — LVH is defined as an increase in the mass of the left ventricle, which can be secondary to an increase in wall thickness or muscle mass. This increase in mass predominantly results from a chronic increase in LV afterload or a primary disease of the myocardium (eg, hypertrophic cardiomyopathy) (see "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Hypertrophic cardiomyopathy: Gene mutations and clinical genetic testing"). In addition to the increased muscle mass, myocardial fibrosis is often present and may contribute to the arrhythmias seen with LVH. In addition, LVH may result in diastolic dysfunction and diastolic heart failure (ie, heart failure with preserved ejection fraction). (See "Pathophysiology of heart failure with preserved ejection fraction".)

LV mass can be estimated using various imaging techniques, including echocardiography and CMR imaging (table 1).

LVH can also be defined electrocardiographically, with the most common findings including increased QRS voltage, increased QRS duration, physiologic left axis deviation (between 0 to -30 degrees), repolarization abnormalities, and left atrial abnormalities. The electrocardiographic diagnosis of LVH is discussed in detail separately. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)

LVH occurs as a physiologic adaptation to increased myocardial wall stress. Typically, LVH results from increases in LV pressures due to increased afterload, most commonly from hypertension or aortic stenosis, although less common causes of increased afterload (eg, coarctation of the aorta, supraaortic or subaortic membranes) may also result in LVH. LVH resulting from pressure overload most commonly results in thickening of the LV walls with normal or reduced LV cavity size. In addition to pressure overload conditions, increased LV mass can result from chronic volume overload conditions (eg, aortic regurgitation, mitral regurgitation, dilated cardiomyopathy), although these conditions typically result in normal to thicker than normal LV walls with increased LV cavity size.

Asymmetric LVH (eg, hypertrophy more prominent in the ventricular septum or apex) may also result from hypertrophic cardiomyopathy, a genetically determined heart muscle disease caused by mutations in one of several sarcomere genes that encode components of the contractile apparatus, with variable phenotypic expressions and clinical manifestations. The unique risks associated with hypertrophic cardiomyopathy are discussed separately. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death" and "Hypertrophic cardiomyopathy in adults: Supraventricular tachycardias including atrial fibrillation".)

LVH frequently occurs as a normal physiologic response to extreme and frequent exercise, such as in highly-trained athletes, and often must be distinguished from pathologic LVH due to other conditions (most commonly hypertrophic cardiomyopathy). LVH in athletes is typically concentric with isometric exercise and eccentric with endurance sports [7-9]. Myocardial fibrosis is generally not present. The mechanisms accounting for LVH in these situations and the consequences of LVH are quite different from those in LVH due to hypertension or valvular heart disease [10,11]. Both systolic and diastolic function are generally maintained in LVH occurring in athletes [8]. The arrhythmias that are seen in athletes who do not have associated cardiac abnormalities are similar in type and frequency to those that occur in the general population [12]. Moreover, in athletes, there is no relationship between arrhythmia and the degree of physiologic LVH [13]. Some of the arrhythmias, such as sinus bradycardia and sinus arrhythmia, are the result of enhanced vagal tone. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Athletes with arrhythmias: Treatment and returning to athletic participation".)

MAKING THE DIAGNOSIS OF LVH — LVH can be diagnosed from a 12-lead ECG or by cardiac imaging, traditionally using echocardiography, but newer imaging modalities such as CMR imaging are also highly effective for calculating cardiac mass. In general, echocardiography and CMR are both more sensitive and more specific than ECG for the diagnosis of LVH, but ECG is more readily available, easy to perform and interpret, and is much less expensive. Imaging the myocardium can also identify specific pathologic features, particularly an eccentric or concentric pattern of LVH. The specific details regarding the diagnosis of LVH with both ECG and imaging modalities are presented separately. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "Transthoracic echocardiography: Normal cardiac anatomy and tomographic views".)

LVH AND VENTRICULAR ARRHYTHMIAS — Patients with evidence of LVH, both electrocardiographic and echocardiographic, are more like to have ventricular ectopy and ventricular tachyarrhythmias compared with normotensive patients or hypertensive patients without LVH [14-22]. Regardless of the method for diagnosing LVH, the presence of LVH is associated with an increased risk for sudden cardiac arrest [23]. In a meta-analysis of 10 studies involving 27,141 patients, the occurrence of ventricular tachycardia or fibrillation was significantly greater in the presence of LVH (odds ratio 2.8 compared with no LVH; 95% CI 1.8-4.5) [2].

The frequency and complexity of ventricular premature beats (VPBs) is related to the severity of LVH as well as chamber volume and indices of left ventricular contractility [18,19]. For every 1 mm increase in wall thickness, there was a two to threefold increase in the occurrence and complexity of VPBs [18]. In addition, several studies have suggested that complex ventricular ectopy, especially nonsustained ventricular tachycardia, is predictive of an increased risk of all-cause mortality [24-26].

LVH AND SUPRAVENTRICULAR ARRHYTHMIAS — Patients with LVH have an increased risk of supraventricular arrhythmias, primarily atrial fibrillation (AF). This is generally due to an increase in left atrial size and/or an increase in left atrial pressure with stretch on the left atrial myocardium. In addition, there is an increase in left atrial muscle mass (hypertrophy) with fibrosis. This results from the thickness and rigidity of the left ventricular myocardium with the occurrence of diastolic dysfunction and the increase in left atrial pressure in order to maintain left ventricular filling during diastole. In a meta-analysis of 10 studies involving 27,141 patients, the occurrence of supraventricular arrhythmias was significantly greater in patients with LVH (odds ratio 3.4 compared with no LVH; 95% CI 1.6-7.3), although there was significant heterogeneity among the baseline covariates in the included studies [2].

The relationship between LVH and AF is well established. The importance of LVH in the development AF was illustrated in a study of 2482 subjects with primary hypertension (formerly called "essential" hypertension) followed for up to 16 years [27]. During follow-up, in which 61 patients developed AF (0.46 per 100 person years), advancing age and increased LV mass were the only independent predictors of developing AF. For every one standard deviation increase on left ventricular mass, the risk of AF increased by 20 percent.

LVH identified by cardiac magnetic resonance imaging has also been shown to be associated with AF. In a cohort of 4942 patients followed for a median of 6.9 years, the risk of AF was significantly greater in patients with LVH identified by either magnetic resonance imaging or electrocardiogram (ECG)-derived voltage measurements of LVH [28].

Additionally, there appears to be an increased risk of sudden cardiac death (SCD) in patients with ECG evidence of LVH who develop AF [29]. (See 'LVH and risk of sudden cardiac death' below.)

LVH AND RISK OF SUDDEN CARDIAC DEATH — LVH is a risk factor for SCD as well as overall cardiovascular mortality, as shown in the following examples:

In a nationwide study of SCD occurring in persons aged 15 to 35 years in Ireland between 2005 and 2007, 10 percent (12 of 116 autopsy-adjudicated cases) had evidence of LVH that did not meet the criteria for another diagnosis (eg, hypertrophic cardiomyopathy) [30].

Among 3661 subjects over the age of 40 from the Framingham Heart Study in whom the relationship between left ventricular mass and hypertrophy and SCD was investigated, the prevalence of LVH was 22 percent [31]. Over an average follow-up of 14 years, patients with LVH had a significantly greater risk of SCD (adjusted hazard ratio 2.2 compared with no LVH; 95% CI 1.2-3.8), with a 50 percent increase in SCD risk for each 50 g/m2 increase in left ventricular mass.

Among a cohort of 8831 hypertensive patients with baseline sinus rhythm and ECG evidence of LVH who were followed for an average of 4.7 years, 701 (7.9 percent) patients developed atrial fibrillation (AF), and 151 patients (1.7 percent) experienced SCD [29]. Multivariate analysis revealed a greater than threefold increased risk of SCD among patients who developed AF (hazard ratio 3.1 compared with those who remained in sinus rhythm, 95% CI 1.9-5.2).

MECHANISMS OF ARRHYTHMIAS IN LVH — Little is known about the physiologic mechanisms accounting for ventricular arrhythmia in LVH. Several theories have been proposed, although it seems likely that the arrhythmogenicity of LVH is multifactorial in origin.

Ischemia — LVH and hypertension without LVH are commonly associated with myocardial ischemia, particularly chronic subendocardial ischemia, accounting for the presence of ST-T wave changes that are often seen with LVH; in addition, microvascular angina can occur in patients with hypertension even in the absence of LVH [32-36]. Several factors can contribute to the development of myocardial ischemia:

A reduction in subendocardial blood flow due to the increase in left ventricular end-diastolic blood pressure. The repolarization changes seen with LVH reflect this reduction in subendocardial blood flow. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis", section on 'Electrocardiographic findings: General'.)

Increased peripheral vascular resistance and an overall reduction in coronary artery blood flow resulting from augmented vasoconstrictor tone and the increased wall/lumen ratio.

Failure of the coronary arteries to grow at a rate sufficient to compensate for the muscular hypertrophy, resulting in decreased coronary reserve and chronic ischemia, a well-recognized stimulus for arrhythmias of all type [36].

Increased oxygen demand due to the rise in wall tension and the increase in myocardial wall thickness, resulting in a reduction in oxygen supply, particularly to the subendocardial layer.

Electrophysiologic abnormalities — The irregular hypertrophy pattern and local areas of fibrosis in LVH can impede the homogeneous propagation of the electric impulse throughout the myocardium and its subsequent recovery [37-40]. Fibrosis is one of the deleterious anatomic abnormalities associated with LVH and may be the main substrate for the development of ventricular arrhythmias, particularly reentrant arrhythmias [21]. Other proposed mechanisms of arrhythmias include lengthening of the action potential duration, reduced action potential upstroke velocity, slower membrane repolarization, the generation of early and delayed afterdepolarizations, and beat-to-beat changes in repolarization [41,42]. In an animal model, the presence of LVH is associated with an increase in transmural repolarization dispersion and the occurrence of early afterdepolarization, which increase the potential for ventricular tachyarrhythmias [43]. (See "T wave (repolarization) alternans: Overview of technical aspects and clinical applications".)

Abnormalities of the hypertrophied myocardial cell — The hypertrophied cardiac myocyte is electrophysiologically different from and more arrhythmogenic than the normal myocyte [38,44]. A number of structural changes that occur in hypertrophy have been related to the susceptibility of the hypertrophied myocardium to arrhythmias. Whether these structural changes correlate with the above electrophysiologic abnormalities is not known.

Increased sympathetic activity — Increased activity of the sympathetic nervous system and the renin-angiotensin system has been implicated in the pathogenesis of primary hypertension (formerly called "essential" hypertension). One study found that abnormal circadian blood pressure variations, as assessed by 24-hour blood pressure monitoring, correlated with the presence of echocardiographic LVH [45]. Thus, at any given level of blood pressure, sympathetic/parasympathetic imbalance may influence the development of LVH and the occurrence of atrial and ventricular arrhythmias. In addition, sympathetic stimulation exerts a direct proarrhythmic effect by enhancing automaticity [46,47]. (See "Enhanced cardiac automaticity".)

REGRESSION OF LVH — In general, lowering blood pressure with antihypertensive agents, weight loss, or dietary sodium restriction decreases cardiac mass in patients with LVH. However, fibrosis, if present, is not reversible. The degree of hypertrophy in patients with hypertension can be reduced by specific antihypertensive therapy, although not all antihypertensive drugs are equipotent in this regard. Regression of LVH diminishes LVH-associated arrhythmias and appears to reduce the risk of sudden cardiac death (SCD). The effect of various blood pressure lowering agents on the incidence of atrial fibrillation (AF) is, however, less certain.

Effect on atrial fibrillation — Data strongly suggest that regression of LVH results in a reduction in the frequency of paroxysmal AF, perhaps mechanistically due to a reduction in left atrial pressure and diameter [48]. There is also a reduction in the likelihood of new onset AF [49].

The effect of various blood pressure lowering agents on the incidence of AF is, however, less certain. In a meta-analysis of 56,308 patients the use of angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) was associated with a significant 28 percent reduction in the relative risk of AF. Reduction in AF was similar between the two classes of drugs (ACEI 28 percent, ARB 29 percent) and was greatest in patients with heart failure [50]. However, there was no significant reduction in AF in patients with hypertension.

Effect on ventricular arrhythmias — Regression of LVH appears to be associated with a reduction in ventricular arrhythmia. In animal models, regression of hypertrophy normalized action potential duration and dispersion of refractoriness and decreased vulnerability to inducible polymorphic ventricular tachycardia (VT) and ventricular fibrillation [51,52].

In trials of various antihypertensive agents, improved blood pressure control was generally associated with regression of LVH and reduction in ventricular ectopy and tachyarrhythmias, although the effect was not consistent among all classes of drugs (notably thiazide diuretics, which were less efficacious) [53-56].

In a trial of 46 hypertensive patients randomly assigned to therapy with enalapril, hydrochlorothiazide, atenolol, or verapamil, in which all drugs significantly lowered blood pressure, LV mass index and ventricular ectopy were reduced by enalapril, atenolol, and verapamil but not hydrochlorothiazide [54]. Similar lack of efficacy with hydrochlorothiazide was previously reported [53].

In a randomized trial of captopril compared with placebo in 27 hypertensive patients with LVH, captopril was associated with a marked reduction in LVH and a marked reduction in ventricular ectopy, whereas the placebo group showed progression of LVH without change in ventricular ectopy [55].

In a randomized trial of 45 hypertensive patients, isradipine (a calcium channel blocker), spirapril (an ACE inhibitor), and the combination produced an equivalent degree of LVH regression and reduction in ventricular ectopy [56].

Based upon the combination of animal and human data, it seems likely that the decrease in ventricular ectopy associated with regression of LVH is not related to a direct antiarrhythmic effect of antihypertensive therapy but to its effects on hemodynamics and perhaps neurohormonal activation.

Effect on sudden cardiac death — Studies of the effects of the regression of LVH on cardiovascular morbidity and mortality are limited; they generally support but do not prove an improvement in outcome beyond that associated with the reduction in blood pressure alone [37,57,58].

Reports from the Framingham Heart Study showed that regression of LVH, as assessed by electrocardiographic criteria, was associated with reductions in the risk of SCD, acute myocardial infarction, and congestive heart failure [59]. Further support for the benefit of LVH regression on SCD comes from a post hoc analysis of the LIFE trial, which enrolled 9193 patients with hypertension and ECG evidence of LVH and randomly assigned them to treatment with atenolol or losartan [60,61]. Over a mean follow-up of 4.8 years, absence of ECG evidence of LVH while on treatment was associated with a significant reduction in the risk of SCD, independent of treatment modality, blood pressure reduction, and other cardiovascular risk factors [60].

SUMMARY

Definition – Left ventricular hypertrophy (LVH), defined as an increase in the mass of the left ventricle, is a common finding in patients with cardiovascular disease (CVD) and CVD risk factors, and it can be diagnosed either by ECG or by echocardiography. (See 'Introduction' above and 'Definition and etiologies of LVH' above.)

Diagnosis – LVH can be diagnosed from a 12-lead ECG or by cardiac imaging, traditionally using echocardiography, but newer imaging modalities such as cardiovascular magnetic resonance (CMR) imaging are also highly effective for calculating cardiac mass. In general, echocardiography and CMR are both more sensitive and more specific than ECG for the diagnosis of LVH, but ECG is more readily available, easy to perform and interpret, and is much less expensive. (See 'Making the diagnosis of LVH' above and "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "Transthoracic echocardiography: Normal cardiac anatomy and tomographic views".)

Arrhythmias – Patients with LVH are more likely to have ventricular ectopy, ventricular tachyarrhythmias, and sudden cardiac arrest compared with normotensive patients or hypertensive patients without LVH. Patients with LVH also have an increased risk of supraventricular arrhythmias, primarily atrial fibrillation. (See 'LVH and ventricular arrhythmias' above and 'LVH and supraventricular arrhythmias' above.)

Mechanisms of arrhythmias in LVH – Little is known about the physiologic mechanisms accounting for ventricular arrhythmia in LVH. Several theories have been proposed, although it seems likely that the arrhythmogenicity of LVH is multifactorial in origin. (See 'Mechanisms of arrhythmias in LVH' above.)

Regression of LVH – In general, lowering blood pressure with antihypertensive agents, weight loss, or dietary sodium restriction decreases cardiac mass in patients with LVH. The degree of hypertrophy in patients with hypertension can be reduced by specific antihypertensive therapy, although not all antihypertensive drugs are equipotent in this regard. (See 'Regression of LVH' above.)

  1. Elias MF, Sullivan LM, Elias PK, et al. Left ventricular mass, blood pressure, and lowered cognitive performance in the Framingham offspring. Hypertension 2007; 49:439.
  2. Chatterjee S, Bavishi C, Sardar P, et al. Meta-analysis of left ventricular hypertrophy and sustained arrhythmias. Am J Cardiol 2014; 114:1049.
  3. Kannel WB, Gordon T, Offutt D. Left ventricular hypertrophy by electrocardiogram. Prevalence, incidence, and mortality in the Framingham study. Ann Intern Med 1969; 71:89.
  4. Kannel WB, Doyle JT, McNamara PM, et al. Precursors of sudden coronary death. Factors related to the incidence of sudden death. Circulation 1975; 51:606.
  5. Kannel WB, Gordon T, Castelli WP, Margolis JR. Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease. The Framingham study. Ann Intern Med 1970; 72:813.
  6. Kannel WB, Castelli WP, McNamara PM, et al. Role of blood pressure in the development of congestive heart failure. The Framingham study. N Engl J Med 1972; 287:781.
  7. Fagard RH. Impact of different sports and training on cardiac structure and function. Cardiol Clin 1997; 15:397.
  8. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The athlete's heart. A meta-analysis of cardiac structure and function. Circulation 2000; 101:336.
  9. Abernethy WB, Choo JK, Hutter AM Jr. Echocardiographic characteristics of professional football players. J Am Coll Cardiol 2003; 41:280.
  10. Cuspidi C, Lonati L, Sampieri L, et al. Similarities and differences in structural and functional changes of left ventricle and carotid arteries in young borderline hypertensives and in athletes. J Hypertens 1996; 14:759.
  11. Di Bello V, Pedrinelli R, Giorgi D, et al. Ultrasonic videodensitometric analysis of two different models of left ventricular hypertrophy. Athlete's heart and hypertension. Hypertension 1997; 29:937.
  12. Zehender M, Meinertz T, Keul J, Just H. ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. Am Heart J 1990; 119:1378.
  13. Biffi A, Maron BJ, Di Giacinto B, et al. Relation between training-induced left ventricular hypertrophy and risk for ventricular tachyarrhythmias in elite athletes. Am J Cardiol 2008; 101:1792.
  14. McLenachan JM, Henderson E, Morris KI, Dargie HJ. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med 1987; 317:787.
  15. Levy D, Anderson KM, Savage DD, et al. Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol 1987; 60:560.
  16. Siegel D, Cheitlin MD, Black DM, et al. Risk of ventricular arrhythmias in hypertensive men with left ventricular hypertrophy. Am J Cardiol 1990; 65:742.
  17. Vester EG, Kuhls S, Ochiulet-Vester J, et al. Electrophysiological and therapeutic implications of cardiac arrhythmias in hypertension. Eur Heart J 1992; 13 Suppl D:70.
  18. Ghali JK, Kadakia S, Cooper RS, Liao YL. Impact of left ventricular hypertrophy on ventricular arrhythmias in the absence of coronary artery disease. J Am Coll Cardiol 1991; 17:1277.
  19. Schmieder RE, Messerli FH. Determinants of ventricular ectopy in hypertensive cardiac hypertrophy. Am Heart J 1992; 123:89.
  20. Novo S, Barbagallo M, Abrignani MG, et al. Increased prevalence of cardiac arrhythmias and transient episodes of myocardial ischemia in hypertensives with left ventricular hypertrophy but without clinical history of coronary heart disease. Am J Hypertens 1997; 10:843.
  21. Mammarella A, Paradiso M, Basili S, et al. Morphologic left ventricular patterns and prevalence of high-grade ventricular arrhythmias in the normotensive and hypertensive elderly. Adv Ther 2000; 17:222.
  22. Palmiero P, Maiello M. Ventricular arrhythmias and left ventricular hypertrophy in essential hypertension. Minerva Cardioangiol 2000; 48:427.
  23. Narayanan K, Reinier K, Teodorescu C, et al. Electrocardiographic versus echocardiographic left ventricular hypertrophy and sudden cardiac arrest in the community. Heart Rhythm 2014; 11:1040.
  24. Bikkina M, Larson MG, Levy D. Asymptomatic ventricular arrhythmias and mortality risk in subjects with left ventricular hypertrophy. J Am Coll Cardiol 1993; 22:1111.
  25. Aronow WS, Epstein S, Koenigsberg M, Schwartz KS. Usefulness of echocardiographic left ventricular hypertrophy, ventricular tachycardia and complex ventricular arrhythmias in predicting ventricular fibrillation or sudden cardiac death in elderly patients. Am J Cardiol 1988; 62:1124.
  26. Saadehm Anm Joes, JV . Predictors of sudden cardiac death in never previously treated patients with essential hypertension: long-term follow up. J Hum Hypertens 2001; 15:667.
  27. Verdecchia P, Reboldi G, Gattobigio R, et al. Atrial fibrillation in hypertension: predictors and outcome. Hypertension 2003; 41:218.
  28. Chrispin J, Jain A, Soliman EZ, et al. Association of electrocardiographic and imaging surrogates of left ventricular hypertrophy with incident atrial fibrillation: MESA (Multi-Ethnic Study of Atherosclerosis). J Am Coll Cardiol 2014; 63:2007.
  29. Okin PM, Bang CN, Wachtell K, et al. Relationship of sudden cardiac death to new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy. Circ Arrhythm Electrophysiol 2013; 6:243.
  30. Margey R, Roy A, Tobin S, et al. Sudden cardiac death in 14- to 35-year olds in Ireland from 2005 to 2007: a retrospective registry. Europace 2011; 13:1411.
  31. Haider AW, Larson MG, Benjamin EJ, Levy D. Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death. J Am Coll Cardiol 1998; 32:1454.
  32. O'Gorman DJ, Sheridan DJ. Abnormalities of the coronary circulation associated with left ventricular hypertrophy. Clin Sci (Lond) 1991; 81:703.
  33. Houghton JL, Prisant LM, Carr AA, et al. Relationship of left ventricular mass to impairment of coronary vasodilator reserve in hypertensive heart disease. Am Heart J 1991; 121:1107.
  34. Lucarini AR, Picano E, Salvetti A. Coronary microvascular disease in hypertensives. Clin Exp Hypertens A 1992; 14:55.
  35. Houghton JL, Carr AA, Prisant LM, et al. Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia. Am J Cardiol 1992; 69:219.
  36. Harrison DG, Marcus ML, Dellsperger KC, et al. Pathophysiology of myocardial perfusion in hypertension. Circulation 1991; 83:III14.
  37. Koren MJ, Devereux RB, Casale PN, et al. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114:345.
  38. Swynghedauw B, Chevalier B, Charlemagne D, et al. Cardiac hypertrophy, arrhythmogenicity and the new myocardial phenotype. II. The cellular adaptational process. Cardiovasc Res 1997; 35:6.
  39. Levy D, Anderson KM, Plehn J, et al. Echocardiographically determined left ventricular structural and functional correlates of complex or frequent ventricular arrhythmias on one-hour ambulatory electrocardiographic monitoring. Am J Cardiol 1987; 59:836.
  40. McLenachan JM, Dargie HJ. Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis. Am J Hypertens 1990; 3:735.
  41. Gillis AM, Mathison HJ, Kulisz E, Lester WM. Dispersion of ventricular repolarization and ventricular fibrillation in left ventricular hypertrophy: influence of selective potassium channel blockers. J Pharmacol Exp Ther 2000; 292:381.
  42. Hennersdorf MG, Niebch V, Perings C, Strauer BE. T wave alternans and ventricular arrhythmias in arterial hypertension. Hypertension 2001; 37:199.
  43. Yan GX, Rials SJ, Wu Y, et al. Ventricular hypertrophy amplifies transmural repolarization dispersion and induces early afterdepolarization. Am J Physiol Heart Circ Physiol 2001; 281:H1968.
  44. Toyoshima H, Park YD, Ishikawa Y, et al. Effect of ventricular hypertrophy on conduction velocity of activation front in the ventricular myocardium. Am J Cardiol 1982; 49:1938.
  45. Verdecchia P, Schillaci G, Guerrieri M, et al. Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension. Circulation 1990; 81:528.
  46. Schwartz PJ, La Rovere MT, Vanoli E. Autonomic nervous system and sudden cardiac death. Experimental basis and clinical observations for post-myocardial infarction risk stratification. Circulation 1992; 85:I77.
  47. Anderson JL, Rodier HE, Green LS. Comparative effects of beta-adrenergic blocking drugs on experimental ventricular fibrillation threshold. Am J Cardiol 1983; 51:1196.
  48. Hennersdorf MG, Schueller PO, Steiner S, Strauer BE. Prevalence of paroxysmal atrial fibrillation depending on the regression of left ventricular hypertrophy in arterial hypertension. Hypertens Res 2007; 30:535.
  49. Okin PM, Wachtell K, Devereux RB, et al. Regression of electrocardiographic left ventricular hypertrophy and decreased incidence of new-onset atrial fibrillation in patients with hypertension. JAMA 2006; 296:1242.
  50. Healey JS, Baranchuk A, Crystal E, et al. Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: a meta-analysis. J Am Coll Cardiol 2005; 45:1832.
  51. Rials SJ, Wu Y, Ford N, et al. Effect of left ventricular hypertrophy and its regression on ventricular electrophysiology and vulnerability to inducible arrhythmia in the feline heart. Circulation 1995; 91:426.
  52. Rials SJ, Wu Y, Xu X, et al. Regression of left ventricular hypertrophy with captopril restores normal ventricular action potential duration, dispersion of refractoriness, and vulnerability to inducible ventricular fibrillation. Circulation 1997; 96:1330.
  53. Messerli FH, Nunez BD, Nunez MM, et al. Hypertension and sudden death. Disparate effects of calcium entry blocker and diuretic therapy on cardiac dysrhythmias. Arch Intern Med 1989; 149:1263.
  54. Novo S, Abrignani MG, Novo G, et al. Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH. Am J Hypertens 2001; 14:637.
  55. González-Fernández RA, Rivera M, Rodríguez PJ, et al. Prevalence of ectopic ventricular activity after left ventricular mass regression. Am J Hypertens 1993; 6:308.
  56. Manolis AJ, Beldekos D, Handanis S, et al. Comparison of spirapril, isradipine, or combination in hypertensive patients with left ventricular hypertrophy: effects on LVH regression and arrhythmogenic propensity. Am J Hypertens 1998; 11:640.
  57. Koren MJ, Devereux RB. Mechanism, effects, and reversal of left ventricular hypertrophy in hypertension. Curr Opin Nephrol Hypertens 1993; 2:87.
  58. Yurenev AP, Dyakonova HG, Novikov ID, et al. Management of essential hypertension in patients with different degrees of left ventricular hypertrophy. Multicenter trial. Am J Hypertens 1992; 5:182S.
  59. Levy D, Salomon M, D'Agostino RB, et al. Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy. Circulation 1994; 90:1786.
  60. Wachtell K, Okin PM, Olsen MH, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive therapy and reduction in sudden cardiac death: the LIFE Study. Circulation 2007; 116:700.
  61. Dahlöf B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 2002; 359:995.
Topic 966 Version 24.0

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