Version July 2025
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 LV myocardium, which can be secondary to an increase in wall thickness or LV muscle mass. If the wall thickness is seen involving all walls of the LV, it is considered to be concentric. If only some walls are involved, such as the septum, it is considered eccentric (eg, hypertrophic cardiomyopathy). (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Hypertrophic cardiomyopathy: Gene mutations and clinical genetic testing".)
In addition to 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 (ie, intraventricular conduction delay), physiologic left axis deviation (between 0 to -30 degrees), repolarization abnormalities (ie, ST-T-wave changes, often referred to as LVH with strain but actually representing chronic subendocardial ischemia due to reduced oxygen supply to the subendocardium), and left atrial abnormalities (ie, broad and notched P wave, termed P-mitral, and/or very negative P wave in leads V1 and V2). Voltage alone is often unreliable, as the QRS voltage recorded on the ECG is also dependent upon body habitus and the presence of lung disease. For example, in a patient with obesity or one with severe chronic obstructive pulmonary disease, LVH may be present, but the QRS voltage may not be increased. In contrast, a young patient who is thin may have voltage criteria for LVH even though LVH may not be present. The ECG diagnosis of LVH is discussed in detail separately. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)
LVH occurs as the result of increased myocardial wall stress or infiltration of the myocardium. 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 in adults: Supraventricular tachycardias including atrial fibrillation" and "Hypertrophic cardiomyopathy: Management of ventricular arrhythmias and sudden cardiac death risk".)
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 or chronic hypertension). 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, either electrocardiographic (ECG) or 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]. However, some have questioned whether such associations are confounded by coronary artery disease [24].
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]. Complex ventricular arrhythmia, primarily nonsustained or sustained ventricular tachycardia, may also be related to the presence of myocardial fibrosis that often occurs with LVH. In addition, several studies have suggested that complex ventricular ectopy, especially nonsustained ventricular tachycardia, is predictive of an increased risk of all-cause mortality [25-27].
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. The stretch on the left atrium or increase in left atrial size can result in an increase in ectopy, which may trigger AF. In addition, there is an increase in left atrial muscle mass (hypertrophy) with fibrosis that often develops, which results from the increase in left atrial pressure during diastole transmitted from the LV. 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 [28]. During follow-up, 61 patients developed AF (0.46 per 100 person years). Advancing age and increased LV mass were the only independent risk factors for development of AF. For every one standard deviation increase on LV mass, the risk of AF increased by 20 percent. Meta-analysis supports this association as well [29].
LVH identified by cardiovascular 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 ECG-derived voltage measurements of LVH [30]. LVH in the presence of elevated biomarkers (high-sensitivity troponin or N-terminal pro-B-type natriuretic peptide), a condition termed "malignant LVH," has particularly been shown to be associated with incident AF [31].
Additionally, there appears to be an increased risk of sudden cardiac death (SCD) in patients with ECG evidence of LVH who develop AF [32]. (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) [33].
●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 [34]. 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 [32]. 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).
However, some have questioned whether these associations may be confounded by coronary artery disease [24].
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 [35-39]. 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 [39].
●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 hypertrophic pattern and local areas of fibrosis in LVH can impede the homogeneous propagation of the electric impulse throughout the myocardium and its subsequent recovery [40-43]. 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 [44,45]. 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 [46]. (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 [41,47]. 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 [48]. 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 [49,50]. (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 generally 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 associated with a reduction in atrial premature complexes [51]. There is also a reduction in the likelihood of new onset AF [52].
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 [53]. 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 and ventricular fibrillation [54,55].
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) [56-59].
●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 [57]. Similar lack of efficacy with hydrochlorothiazide was previously reported [56].
●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 [58].
●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 [59].
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 [40,60,61].
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 [62]. 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 [63,64]. 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 [63].
SUMMARY
●Definition – Left ventricular hypertrophy (LVH), defined as an increase in the mass of the left ventricle, is a common finding in patients with hypertension, cardiovascular disease (CVD) and CVD risk factors, and it can be diagnosed either by ECG or by an imaging modality such as echocardiography or cardiovascular magnetic resonance (CMR) imaging. (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 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 frequent 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.)
