Electrocardiographic Evidence Of Left Ventricular Hypertrophy Research Articles

Direct Stimulation of Cardiogenesis: A New Paradigm for Treating Heart Disease.

Heart failure (HF) is highly prevalent and is associated with substantial mortality and morbidity, despite the many treatment options currently available. We propose a potential new approach to treating heart disease: promoting cardiogenesis from existing cardiac myocytes by inhibiting the Hippo pathway, a stop growth pathway in the heart. HF is the third leading cause of cardiovascular death in the United States. It is a syndrome associated with high mortality, considerable morbidity, and an economic burden that is often relentlessly progressive. The American Heart Association and American College of Cardiology classify HF into 4 stages: stage A, presence of risk factors, but with normal cardiac function and structure; stage B, subclinical changes in left ventricular (LV) structure and function; stage C, clinical HF; and stage D, advanced HF. Coronary artery disease is present in approximately half of patients with new-onset clinical HF and is especially prevalent in patients with a reduced LV ejection fraction. Data from Framingham show a rise in post–myocardial infarction (MI) clinical HF rates between 1971 and 2000, which is primarily due to an increase in HF incidence in the early post-MI period. It has been speculated that because intervention and thrombolytic therapy have improved survival in patients with MI, the population of patients at risk of post-MI HF has grown. Major clinical risk factors for HF include age, male sex, hypertension, electrocardiographic evidence of LV hypertrophy, MI, diabetes mellitus, valvular heart disease, and obesity. …

Clinical Diagnosis of Electrical Versus Anatomic Left Ventricular Hypertrophy: Prognostic and Therapeutic Implications.

Left ventricular hypertrophy (LVH) can develop in association with chronic arterial hypertension and other cardiovascular disorders and is a well-established risk factor for cardiac arrhythmias, cardiovascular events, and mortality.1 Over 4 decades ago the Framingham Heart Study reported that electrocardiographic evidence of LVH (ECG LVH) was associated with 3- to 4-fold increase in cardiovascular and all-cause mortality, with a disproportionately high risk of sudden cardiac death (SCD).2,3 Subsequently, multiple studies in different population samples have confirmed these associations.4,5 In early studies, the 12-lead ECG was the only available method to diagnose LVH in living subjects. In subsequent years, anatomic LVH diagnosed by echocardiography (echo LVH) became the gold standard.6,7 Despite the development of fairly detailed diagnostic ECG criteria for LVH,8 echocardiographic measurements have virtually replaced the ECG diagnosis of LVH. This shift in clinical practice was driven by the low reported sensitivity (usually <25%), albeit high specificity (up to 95%) of ECG criteria for diagnosis of LVH with echocardiography, magnetic resonance imaging (MRI), or during autopsy.9,10 More recently, however, we are learning that ECG LVH and echo LVH may be clinically distinct entities. In fact, there are now data to suggest that although these 2 entities can often overlap, each may provide distinct prognostic and potentially, mechanistic information, especially in the context of cardiac arrhythmias. This review will attempt to put these findings into perspective for the clinical electrophysiologist, by discussing the significance of electrical versus anatomic LVH for occurrence of atrial fibrillation (AF) and SCD. To diagnose increased left ventricular (LV) mass from the 12-lead ECG, over 30 different ECG criteria have been developed. Most of the commonly used LVH criteria, such as Sokolow and Lyon, and Cornell voltage, rely solely on measuring QRS voltage. …

Association between transforming growth factor-β 1 and left ventricular mass and diameter in hypertensive patients

Angiotensin II influences development of left ventricular hypertrophy (LVH) by stimulating cardiomyocyte hypertrophy, fibroblast proliferation, and collagen synthesis. Because pro-fibrotic actions of angiotensin may be mediated by increased production of transforming growth factor-β 1 (TGF-β 1), we assessed whether serum TGF-β 1 levels might reflect involvement in LVH development. We analyzed relationships between left ventricular mass and levels of renin, aldosterone, and TGF-β 1 in 67 hypertensive subjects (mean age 64 ± 11.3 years) with electrocardiographic evidence of LVH. Levels were obtained after a 2-week washout of antihypertensive medications; two-dimensional echocardiography was subsequently performed. Linear regression analysis showed a correlation between TGF-β 1 and LV mass (r = 0.36, P = .002). This was apparently explained by the correlation between TGF-β 1 and left ventricular diastolic internal diameter (r = 0.42, P < .001), because no correlation between TGF-β 1 levels and LV wall thickness was found. In multivariate analysis, the correlation between TGF-β 1 and internal diameter remained significant (r = 0.39, P = .0014). There were no racial differences in levels of TGF-β 1 or left ventricular geometry, and no correlations between age, blood pressure, renin, aldosterone, and left ventricular mass or dimensions. These findings indicate that serum TGF-β 1 levels are related to left ventricular structure in hypertensive subjects, suggesting its possible involvement in the process of hypertensive left ventricular remodeling.

Left ventricular structure in different types of chronic pressure overload

Aims Hypertension and aortic stenosis (AS) are different forms of chronic pressure overload that lead to changes in left ventricular (LV) geometry. This article explores the relationship between LV geometry and outcomes, as well as the distribution of LV geometric patterns in patients with hypertension and those with asymptomatic AS with or without concomitant hypertension. Methods and results Studies describing the distribution of LV geometry, or the relationship between LV geometry and outcome, in patients with hypertension and/ or AS were reviewed. Abnormal LV geometry increases the risk of major cardiovascular events and mortality in patients with untreated hypertension, with concentric hypertrophy conferring the greatest risk, followed by eccentric hypertrophy and then concentric remodelling. Abnormal LV geometry during antihypertensive drug therapy also increases cardiovascular risk compared with normal geometry. In asymptomatic AS, the relationship between LV geometry and outcome remains to be clarified. A pooled analysis of data from two major clinical studies, Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) and Simvastatin and Ezetimibe in Aortic Stenosis (SEAS), showed that the prevalence of abnormal LV geometry increases with increasing chronic pressure overload—from 35% in normotensive patients with asymptomatic mild-to-moderate AS to 80% in patients with hypertension and electrocardiographic evidence of LV hypertrophy (LVH). In patients with asymptomatic AS, concentric LV geometry is most common, whereas eccentric hypertrophy is the most common LV geometric abnormality in patients with hypertension and LVH. Conclusion Abnormal LV geometry has been independently associated with adverse outcomes in hypertension. Patients with asymptomatic mild-to-moderate AS often have abnormal LV geometry irrespective of the presence of concomitant hypertension, and, accordingly, may be at higher cardiovascular risk than expected on the basis of their AS alone. In the future, ongoing clinical trials involving AS patients, such as the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study, may help to provide further information concerning relationships between abnormal LV geometry and clinical outcomes among individuals with asymptomatic AS.

Preventing Left Ventricular Hypertrophy by ACE Inhibition in Hypertensive Patients With Type 2 Diabetes

OBJECTIVE—In patients with type 2 diabetes, left ventricular hypertrophy (LVH) predicts cardiovascular events, and the prevention of LVH is cardioprotective. We sought to compare the effect of ACE versus non-ACE inhibitor therapy on incident electrocardiographic (ECG) evidence of LVH (ECG-LVH).RESEARCH DESIGN AND METHODS—This prespecified study compared the incidence of ECG-LVH by Sokolow-Lyon and Cornell voltage criteria in 816 hypertensive type 2 diabetic patients of the Bergamo Nephrologic Diabetes Complications Trial (BENEDICT), who had no ECG-LVH at baseline and were randomly assigned to at least 3 years of blinded ACE inhibition with trandolapril (2 mg/day) or to non-ACE inhibitor therapy. Treatment was titrated to systolic/diastolic blood pressure <130/80 mmHg. ECG readings were centralized and blinded to treatment.RESULTS—Baseline characteristics of the two groups were similar. Over a median (interquartile range) follow-up of 36 (24–48) months, 13 of the 423 patients (3.1%) receiving trandolapril compared with 31 of the 376 patients (8.2%) receiving non-ACE inhibitor therapy developed ECG-LVH (hazard ratio [HR] 0.34 [95% CI 0.18–0.65], P = 0.0012 unadjusted, and 0.35 [0.18–0.68], P = 0.0018 adjusted for predefined baseline covariates). The HR was significant even after adjustment for follow-up blood pressure and blood pressure reduction versus baseline. Compared with baseline, both Sokolow-Lyon and Cornell voltages significantly decreased with trandolapril but did not change with non-ACE inhibitor therapy.CONCLUSIONS—ACE inhibition has a specific protective effect against the development of ECG-LVH that is additional to its blood pressure–lowering effect. Because ECG-LVH is a strong cardiovascular risk factor in people with hypertension and diabetes, early ACE inhibition may be cardioprotective in this population.

Home-measured blood pressure is more strongly associated with electrocardiographic left ventricular hypertrophy than is clinic blood pressure: the Finn-HOME study

Electrocardiographic evidence of left ventricular hypertrophy (ECG-LVH) has a grave prognostic significance in hypertensive patients. The purpose of our study was to assess whether ECG-LVH is more strongly associated with home-measured blood pressure (BP) than with clinic BP, and whether the correlation between home BP and ECG-LVH increases with the number of home measurements performed. We studied a representative sample of the general adult population (1989 subjects 45-74 years of age) in Finland. Subjects included in the study underwent a clinical interview, electrocardiography and measurement of clinic BP (mean of two clinic measurements) and home BP (mean of 14 duplicate home measurements performed during 1 week). Home BP correlated significantly better than clinic BP with the Sokolow-Lyon voltage (home/clinic systolic: r=0.23/0.22, P=0.60; diastolic: r=0.17/0.12, P=0.009), Cornell voltage (systolic: r=0.30/0.25, P=0.004; diastolic: r=0.21/0.12, P<0.001) and Cornell product (systolic: r=0.30/0.24, P=0.001; diastolic r=0.22/0.14, P<0.001) criteria of ECG-LVH. The correlation between home BP and ECG-LVH increased slightly with the number of home measurements, but even the mean of the initial two home BP measurements correlated equally well (systolic BP), or better (diastolic BP) with ECG-LVH than did clinic BP. In conclusion, home BP measurement allows us to obtain a large number of measurements that have a strong association with ECG-LVH. Our data support the application of home BP measurement in clinical practice.

Should Antihypertensive Therapy Target Both LVH and BP

Electrocardiographic evidence of left-ventricular hypertrophy (LVH) has a well-known association with increased risk for atrial fibrillation (AF). In

Aortic valve sclerosis: new help from echocardiography in the assessment of cardiovascular risk

Aortic valve sclerosis: new help from echocardiography in the assessment of cardiovascular risk

Relation of QT interval and QT dispersion to regression of echocardiographic and electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) study

BackgroundIn hypertensive patients, both echocardiographic and electrocardiographic left ventricular hypertrophy (LVH) increase the risk of sudden death, possibly in part because of LVH-induced proarrhythmic repolarization changes. Experimentally, regression of LVH normalizes ventricular electrophysiology. MethodsTo assess the relation of regression of LVH to changes in electrocardiographic measures of ventricular repolarization, we studied 317 hypertensive (61.2% men, mean age 65 ± 7 years) participants in the Losartan Intervention For Endpoint Reduction (LIFE) study with electrocardiographic evidence of LVH, at study baseline, and after 1 year of blood pressure-lowering treatment with losartan or atenolol and hydrochlorothiatzide as the first adjunct therapy if needed to reach target blood pressure of 140/90 mm Hg. As indexes of LVH, we used echocardiographically determined LV mass as well as the Sokolow-Lyon and Cornell voltages from the electrocardiogram. QT interval duration and QT dispersion from the 12-lead electrocardiogram were used as ventricular repolarization measures. ResultsBy using tertiles of LV mass change and adjusting for the difference in treatment (losartan or atenolol), shortening of the rate-adjusted QT intervals as well as reduction in QTapex dispersion were observed in the tertile showing the greatest decrease in LV mass but not in the tertile without substantial changes in LV mass despite a significant reduction in blood pressure. Similar results were obtained with the use of Sokolow-Lyon and Cornell voltage change tertiles. ConclusionsIn hypertensive patients with electrocardiographic evidence of LVH, regression of echocardiographically determined LV mass and electrocardiographic indexes of LVH may partially reverse the LVH-induced proarrhythmic repolarization changes. This may have a beneficial impact on the increased incidence of sudden death in these patients.

Relation of QT interval and QT dispersion to echocardiographic left ventricular hypertrophy and geometric pattern in hypertensive patients. The LIFE study. The Losartan Intervention For Endpoint Reduction.

In hypertensive patients, left ventricular hypertrophy (LVH) predicts increased mortality, in part due to an increased incidence of sudden death. Repolarization-related arrhythmogenesis may be an important mechanism of sudden death in hypertensive patients with LVH. Increased QT interval and QT dispersion are electrocardiographic (ECG) measures of ventricular repolarization, and also risk markers for ventricular tachyarrhythmias. We assessed the relation of QT intervals and QT dispersion to echocardiographically determined left ventricular (LV) mass and geometry in a large population of hypertensive patients with ECG evidence of LVH. QT intervals and QT dispersion were determined from baseline 12-lead ECGs in 577 (57% male; mean age 65 +/- 7 years) participants in the LIFE study. LV mass index (LVMI) and geometric pattern were determined by echocardiography and QT interval duration and QT dispersion were assessed in relation to gender-specific LVMI quartiles. In both genders, increasing LVMI was associated with longer rate-adjusted QT intervals. QT dispersion measures showed a weaker association with LVMI quartiles. Both concentric and eccentric LVH were associated with increased QT interval duration and QT dispersion. These relations remained significant after controlling for relevant clinical variables. In hypertensive patients with ECG evidence of LVH, increased LVMI and LVH are associated with a prolonged QT interval and increased QT dispersion. These findings suggest that an increased vulnerability to repolarization-related ventricular arrhythmias might in part explain the increased risk of sudden death in hypertensive patients with increased LV mass.

Impact of coronary artery disease on left ventricular systolic function and geometry in hypertensive patients with left ventricular hypertrophy (the LIFE study)

Hypertensive patients with left ventricular (LV) hypertrophy have a higher incidence of cardiovascular events than those without it. We hypothesized that a close relation exists between clinical evidence of coronary artery disease (CAD) and alterations in LV structure and function that contribute to their higher risk. Echocardiograms were recorded in 963 hypertensive patients (mean age 66 ± 7 years, 41% women) with electrocardiographic LV hypertrophy, and divided into 149 with and 814 without clinical (prior myocardial infarction or angina pectoris) or electrocardiographic (Minnesota codes 1.1, 1.2) evidence of CAD. Patients with CAD had larger LV internal dimensions (5.5 ± 0.6 vs 5.2 ± 0.5 cm), increased LV mass (136 ± 31 vs 122 ± 24 g/m2, and 62.4 ± 19.4 vs 55.5 ± 12.1 g/m2.7), lower ejection fraction (58 ± 10% vs 62 ± 8%), higher circumferential end-systolic wall stress (cESS) (198 ± 59 vs 181 ± 47 kdynes/cm2, all p <0.001), and higher total peripheral resistances (2,088 ± 628 vs 1,963 ± 553 dynes · s · m2/cm3, p = 0.02). Although eccentric LV hypertrophy predominated, the CAD group had a greater prevalence of this geometric pattern than the non-CAD group (56% vs 47%, p <0.02). An index of myocardial oxygen demand per beat—the LV mass · cESS · ejection time—was 20% higher in patients with CAD. In conclusion, clinical evidence of CAD in hypertensive patients with electrocardiographic evidence of LV hypertrophy identifies subjects with structural and functional abnormalities at high risk for cardiovascular events. LV mass · cESS · ejection time, a noninvasive index that parallels myocardial oxygen demand per beat, is especially high in hypertensive patients with CAD.

Hypertrophic Cardiomyopathy

ypertrophic cardiomyopathy (HCM) is a fascinatingdisease that has intrigued and challenged cardiolo-gists for decades. Initially a diagnosis made bymaster clinicians adept at translating bedside dynamic aus-cultation into hemodynamic pathophysiology, HCM contin-ues to challenge the frontiers of diagnosis and technology.The development of 2D and Doppler echocardiography pro-vided the greatest increment in understanding the complexityof HCM. While clinicians at large became skilled at thebedside detection of dynamic left ventricular outflow obstruc-tion, echocardiography revealed that many more patients hadunexplained left ventricular hypertrophy (LVH) consistentwith HCM but without evidence of obstruction. In fact, thenonobstructive, “silent” forms are more frequent than theobstructive, “noisy” variants. The pattern and severity ofLVH are now appreciated as heterogeneous and diastolicdysfunction as highly prevalent.

Enhanced prognostic stratification of patients with left ventricular hypertrophy with the use of single-photon emission computed tomography

Background Patients with left ventricular hypertrophy (LVH) are at increased risk of future cardiovascular events. Little is known about risk stratification of these patients with the use of myocardial perfusion imaging. This study sought to assess the prognostic stratification of patients with LVH by using myocardial perfusion single-photon emission computed tomography (SPECT). Methods and Results We studied 633 consecutive patients with electrocardiographic evidence of LVH who underwent dual isotope myocardial perfusion SPECT (rest thallium 201/stress technetium 99m sestamibi) and were followed up for a mean period of 22 ± 7 months. During the follow-up period, 67 events (35 cardiac deaths and 32 nonfatal myocardial infarctions) occurred (6% annual event rate). The results of the perfusion scan significantly risk-stratified the population; patients with normal scans had a low rate of nonfatal myocardial infarction and cardiac death (<1% per year of follow-up). The rates of cardiac events increased significantly as a function of the scan result: 4.9% in patients with mildly abnormal scans and 10.3% in moderately to severely abnormal scans. Cox proportional hazards analysis demonstrated that after adjusting for pretest likelihood of coronary artery disease (the most predictive clinical variable; χ2 = 15.5, P <.001), summed stress score (the most predictive nuclear variable; χ2 = 18, P <.0001) added significant incremental prognostic information (global χ2 increased from 15.5 to 36; P <.001). Conclusions In patients with LVH with an overall high cardiac event rate, SPECT provided enhanced stratification by adding significant incremental prognostic information over clinical and historic variables. (Am Heart J 2000;140:456-62.)

Antihypertensive drug therapy in the third millennium: are there benefits beyond blood pressure?

The classic outcome trials in hypertension, most of which used diuretics and b-blocking agents as first-line antihypertensive agents, have shown that antihypertensive drug treatment greatly reduces the risk of stroke, heart failure, and left ventricular hypertrophy (LVH). However, it is less successful in preventing fatal and nonfatal coronary heart disease (CHD) [1]. In the Framingham Heart Study, increased rates of use of antihypertensive medications, from 2.3% to 24.6% among men and from 5.7% to 27.7% among women, were associated with reduced prevalence of hypertension (blood pressure [BP]>160/100 mm Hg). Reductions were from 18.5% to 9.2% among men and from 28.0% to 7.7% among women. The prevalence of electrocardiographic evidence of LVH, an index of target organ damage, was reduced from 4.5% to 2.5% among men and from 3.6% to 1.1% among women. These findings suggest that the increasing use of antihypertensive medication may in part explain the major decline in mortality from cardiovascular disease observed in the United States since the late 1960s. Yet, despite these effective treatments, many important questions remain, some of which have been addressed by recently completed and ongoing clinical trials: • Are the newer classes of drugs, such as the calciumchannel blockers (CCBs), angiotensin-converting enzyme inhibitors (ACEIs), angiotensin-II type-1 receptor blockers (ARBs), or a-adrenergic blockers (ABs) superior to diuretics or b-blockers in preventing cardiovascular disease and events? • Do specific classes of antihypertensive drugs, over and above their blood pressure–lowering effects, benefit specific subgroups of hypertensive patients? • What is the appropriate BP goal in various patient groups? • Are specific antihypertensive drugs indicated in special groups of patients, such as the very elderly (>80 years), normotensive persons at high cardiovascular risk, patients with type 2 diabetes, patients with stage 1 hypertension, or hypertensive patients of African-American extraction?

Diagnostic usefulness of postexercise systolic blood pressure response for detection of coronary artery disease in patients with electrocardiographic left ventricular hypertrophy

Patients with left ventricular (LV) hypertrophy often have a positive result on exercise testing despite a normal coronary arteriogram. This indicates that exercise-induced ST depression is not always an accurate indicator of the presence of coronary artery disease (CAD) in such patients. We evaluated the usefulness of the postexercise systolic blood pressure (BP) response for detection of CAD in 51 patients with both electrocardiographic evidence of LV hypertrophy and positive ST depression on treadmill exercise testing. Coronary cineangiograms showed normal coronary arteries in 23 patients (45%) (group 1) and significant CAD in 28 patients (55%) (group 2). The systolic BP ratio (systolic BP at 3 minutes of recovery divided by systolic BP at peak exercise) was significantly higher in group 2 than in group 1 (1.01 ± 0.19 vs 0.80 ± 0.09; p < 0.001). Analysis of the relative cumulative frequency revealed that a systolic BP ratio of 0.86 was the cutoff point for distinguishing a patient with CAD from one with normal coronary arteries. The sensitivity, specificity, and accuracy of a systolic BP ratio ≥0.86 for detection of CAD in patients with LV hypertrophy were 79%, 83%, and 82%, respectively. Our results suggest that the use of an abnormal BP ratio, in combination with ST depression, improves the accuracy of treadmill exercise testing for detecting CAD in patients with electrocardiographic evidence of LV hypertrophy.

The utility of clinical, electrocardiographic, and roentgenographic variables in the prediction of left ventricular function

To determine the clinical value of simple, widely available variables in estimating left ventricular (LV) function, we performed an analysis on 14,507 patients presenting with chest pain who were enrolled in the Coronary Artery Surgery Study registry. Of these patients, 4,034 had a normal electrocardiogram, and of these, 91.8% had an LV ejection fraction (EF) >0.50, 7.6% had an EF of 0.36 to 0.50, and only 0.6% had an EF ≤0.35. The presence of T-wave abnormalities (with normal QRS), left bundle branch block, electrocardiographic evidence of LV hypertrophy or myocardial infarction, cardiomegaly on chest roentgenogram, basilar rales, or third heart sound significantly decreased the likelihood of normal LVEF. Based on these clinical variables, a logistic regression model with a sensitivity of 68% and a specificity of 74% for identifying subjects with normal EF was developed. It was concluded that in patients with chest pain, consideration of such readily available clinical data provides useful information and may decrease the need for more expensive imaging methods.

Pathophysiology and clinical aspects of hypertensive hypertrophy.

Individuals with hypertension and electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) have a 10-fold greater risk of developing cardiac failure than hypertensives without ECG evidence of LVH. LVH in hypertension is characterized by myocardial fibrosis and structural changes to the small intramural arteries. Hypertensives with or without LVH have reduced coronary vasodilator reserve due to hypertensive disease of small coronary arteries. Prognosis of arterial hypertension is largely determined by cardiac complications. The aim of treatment of hypertensive heart disease is to reverse myocardial hypertrophy in order to prevent progression to hypertensive heart failure, as well as reversal of the hypertensive disease of small coronary arteries in order to improve coronary reserve. On the development of hypertensive heart failure, administration of digitalis, diuretics and angiotensin converting enzyme (ACE) inhibitors should be initiated. Although regression of LVH can be induced by dihydropyridine calcium channel blockers, ACE inhibitors and sympatholytic substances, clinical evidence of the reversal of hypertensive disease of small coronary arteries has still to be established.

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age <50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate >120 beats/min. Patients taking β-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 ± 0.01, normotensive patients 0.70 ± 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 ± 0.01, normotensive patients 0.07 ± 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 ± 3 ml/m 2, normotensive -10 ± 1 ml/m 2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.

Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased?

The Framingham Study has indicated that patients with left ventricular hypertrophy (LVH) have a greater risk of cardiovascular complications and sudden death than subjects with a normal heart. We have previously demonstrated that ventricular ectopy was more prevalent and complex in hypertensive patients with LVH by electrocardiographic (ECG) criteria than in those without ECG evidence of LVH. The present study was designed to detect and quantify ventricular dysrhythmias in hypertensive patients with early concentric LVH by echocardiography but without LVH by ECG criteria. Continuous ambulatory ECG tracings were recorded for 24 hours in 94 patients with essential hypertension: 37 without LVH, 26 with concentric LVH by echocardiographic but not ECG criteria, and 31 with LVH on both echocardiography and ECG. Patients with LVH by ECG criteria had significantly more premature ventricular contractions (P less than .001) and more complex (higher Lown's class) ventricular ectopy (P less than .001) than hypertensives without LVH or with LVH only by echocardiographic criteria. Prevalence and complexity of ventricular ectopic activity, however, was not affected by mild to moderate concentric cardiac hypertrophy detected echocardiographically. We conclude that unlike LVH shown by ECG, early hypertensive concentric LVH detected echocardiographically is not associated with increased electrical irritability of the myocardium.

Left ventricular hypertrophy, arrhythmias and sudden death in systemic hypertension

Left ventricular (LV) hypertrophy is a significant independent risk factor for mortality from coronary heart disease, including sudden death. The proportion of sudden death to total death due to coronary heart disease remains high, at about 50% to 60%, despite the continuing downward trend in coronary heart disease mortality observed in the U.S. during the last decade. Prevalence of LV hypertrophy, determined by electrocardiogram in hypertensive patients (diastolic blood pressure ≥ 90 mm Hg), including tall R wave and evidence of repolarization abnormality, is around 5%. The prevalence of LV hypertrophy by echocardiography is estimated at 44% to 48%. LV hypertrophy on electrocardiogram underestimates the magnitude of the problem of LV hypertrophy in hypertensive patients. Its overall sensitivity is < 60%. The incidence of LV hypertrophy in hypertensive patients is lower when hypertension is treated successfully than when the patient is left either untreated or inadequately treated; successful treatment of hypertension causes regression of LV hypertrophy. However, hypertensive patients with LV hypertrophy have a poor prognosis despite treatment. The available evidence derived from the results of large clinical trials suggests that hypertensive patients should be treated before there is electrocardiographic evidence of LV hypertrophy.