[Cardiac hypertrophy, ventricular hypertrophy (left ventricular hypertrophy, right ventricular hypertrophy, combined ventricular hypertrophy)].
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Cardiomegaly↗
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A case of atrial septal defect combined with hypertension and left ventricular hypertrophy. Left ventricular failure induced by balloon occlusion and the effect of nifedipine.
A 46 year old woman with hypertension and left ventricular hypertrophy accompanied by an atrial septal defect is reported. Hemodynamic changes induced by balloon occlusion and concomitant nifedipine were studied. Left ventricular failure appeared after balloon closure of the defect. Nifedipine decreased the increment in left ventricular end-diastolic pressure induced by balloon occlusion. After the reduction of systemic vascular resistance, the ratio of intracardiac shunt flow was still larger. Surgical closure of the defect was performed and the postoperative course was good with the use of vasodilators.
Blood Pressure↗
24-h Ambulatory blood pressure in patients with ECG-determined left ventricular hypertrophy: left ventricular geometry and urinary albumin excretion-a LIFE substudy.
This study was undertaken to evaluate the relationships among left ventricular (LV) geometric patterns and urinary albumin excretion in patients with hypertension and electrocardiographic (ECG) LV hypertrophy. In 143 patients with stage II-III hypertension, 24-h ambulatory blood pressure (BP) monitoring, single urine albumin determination, and echocardiography were performed after 14 days of placebo treatment. Mean age was 68+/-7 years, 35% were women, body mass index was 28+/-5 kg/m(2), LV mass index (LVMI) was 125+/-26 g/m(2), and 24% had microalbuminuria. The mean office BP was 176+/-15/99+/-8 mmHg and the mean daytime ambulatory BP was 161+/-18/92+/-12 mmHg. Ambulatory BP, but not office BP, was higher among albuminuric compared to normoalbuminuric patients. In patients with established hypertension, daytime pulse pressure and office BP were different in the four patterns of LV geometry, with the highest pressure in those with abnormal geometry. Furthermore, microalbuminuria was more frequent in hypertensive patients with LV hypertrophy than in those with either normal geometry or concentric remodelling. White coat hypertensives (10%) showed lower LVMI and no microalbuminuria compared to patients with established hypertension. There were no differences in the prevalence of nondippers (26%) among the four LV geometric patterns or in microalbuminuria. In conclusion, increased daytime pulse pressure and office BP were associated with increased prevalence of abnormal LV geometry. Microalbuminuria was more frequent in groups with concentric and eccentric LV hypertrophy. Ambulatory BP, but not office BP, was higher in albuminuric than normoalbuminuric patients. With regard to the relationship among BP, LV geometric patterns, and urine albumin excretion in this population, 24-h ambulatory BP did not provide additional information beyond the office BP.
Aged↗
Dispersion of the QT interval and autonomic modulation of heart rate in hypertensive men with and without left ventricular hypertrophy.
Left ventricular hypertrophy is an independent risk factor for sudden cardiac death in hypertension, but the mechanisms of electrical instability associated with hypertrophy are not well known. We studied dispersion of the QT interval, an index of inhomogeneity of repolarization, and heart rate variability, a measure of cardiac autonomic modulation, in a randomly selected population of 162 men with systemic hypertension and made comparisons between the patients with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index > or = 131 g/m2, n = 44) and those without hypertrophy (left ventricular mass index < 131 g/m2, n = 118). The heart rate-corrected QT dispersion (67 +/- 37 versus 53 +/- 21 milliseconds, P < .05) and QT apex dispersion (55 +/- 22 versus 44 +/- 16 milliseconds, P < .01) were significantly longer in the patients with left ventricular hypertrophy than in those without hypertrophy. Thirteen of the 44 patients (30%) with hypertrophy versus 7 of the 118 patients (6%) without hypertrophy had an abnormally long QT apex dispersion ( > 70 milliseconds) (P < .001). The time and frequency domain measures of heart rate variability did not differ significantly between the patient groups with and without left ventricular hypertrophy. The measures of heart rate variability were not related to QT dispersion or left ventricular mass index but had a negative correlation with blood pressure values (eg, r = -.30 between the low-frequency component of heart rate variability and systolic pressure, P < .001). Age, body mass index, antihypertensive medication, and the other demographic variables were similar between the groups, but the patients with left ventricular hypertrophy had higher systolic (P < .01) and diastolic (P < .01) pressures compared with the patients without hypertrophy. Left ventricular hypertrophy in hypertensive men is associated with inhomogeneity of the early phase of ventricular repolarization, favoring susceptibility to reentrant ventricular tachyarrhythmias. Abnormalities in cardiac autonomic function, which may trigger a spontaneous onset of arrhythmias, are related to elevated blood pressure but not specifically to left ventricular hypertrophy.
Adult↗
Development and regression of left ventricular hypertrophy.
Left ventricular hypertrophy is an important adaptive response to chronic pressure or volume overload of the left ventricle. The different types and the pathophysiologic mechanisms of the development of left ventricular hypertrophy in various disease states are reviewed. Detection of left ventricular hypertrophy may be accomplished by electrocardiography and cardiac angiography. Echocardiography, however, is the most accurate noninvasive method to detect the presence and estimate the severity of increased left ventricular mass. The clinical significance of left ventricular hypertrophy and its prognostic implications in several cardiac diseases associated with hypertrophy are discussed. The critical transition stage from adaptive, compensatory and reversible left ventricular hypertrophy to "pathologic" hypertrophy with impaired left ventricular contractility and irreversible myocardial damage is yet unknown. Recent data are presented that provide evidence of regression of left ventricular hypertrophy after medical treatment of patients with hypertension and after aortic valve replacement in patients with aortic valve disease. The clinical importance of regression of hypertrophy and its effects on long-term prognosis remain to be determined.
Animals↗
New developments in the epidemiology of left ventricular hypertrophy.
Left ventricular hypertrophy is associated with an increased risk of coronary heart disease and all-cause mortality. Electrocardiographic criteria for left ventricular hypertrophy have high specificity but low sensitivity. Recent advances in methodology have improved the sensitivity of the electrocardiogram for detecting left ventricular hypertrophy. Criteria for left ventricular hypertrophy have been developed from epidemiologic studies using M-mode echocardiography. The prevalence of left ventricular hypertrophy is influenced by blood pressure, age, sex, and obesity. Recent studies have shown that waist-to-hip ratio, hyperinsulinemia, a dominant late systolic peak in the arterial pressure waveform, and a decrease in nocturnal blood pressure decline are also determinants of left ventricular mass. Left ventricular hypertrophy is associated with an increased incidence of ventricular arrhythmias and with an impairment in coronary flow reserve. Newer imaging techniques, such as two- and three-dimensional echocardiography, magnetic resonance imaging, and ultra-fast computed tomography are more accurate and reproducible than M-mode echocardiography, but these methodologies are expensive and not readily available for assessment of left ventricular mass.
Cardiac Volume↗
Prevalence and natural history of electrocardiographic left ventricular hypertrophy.
Left ventricular hypertrophy, particularly on the electrocardiogram, is an ominous, not an incidental accompaniment of hypertension and cardiovascular disease. The prevalence of electrocardiographic left ventricular hypertrophy increases with age with a slight male predominance, and one in 10 persons aged 30 to 62 can expect to have it within 12 years. At any age, cardiac enlargement on roentgenograms is twice as prevalent as electrocardiographic left ventricular hypertrophy, and in only 16 percent of those with x-ray evidence of cardiac enlargement does electrocardiographic left ventricular hypertrophy subsequently develop. Hypertension predisposes and at systolic pressures exceeding 180 mm Hg evidence of electrocardiographic left ventricular hypertrophy develops in 50 percent, with no closer relation to diastolic, than to systolic pressure. In addition to drastic curtailment of life expectancy, electrocardiographic left ventricular hypertrophy is a harbinger of serious cardiovascular disease. Definite electrocardiographic left ventricular hypertrophy is associated with an eightfold increase in cardiovascular mortality and a sixfold increase in coronary mortality. Electrocardiographic left ventricular hypertrophy with repolarization criteria more than doubles the risk of hypertension alone and carries a greater risk of cardiovascular morbidity and mortality than cardiac enlargement. It identifies hypertensive patients with a compromised coronary circulation and myocardial damage. Risk of stroke, cardiac failure, and every clinical manifestation of coronary heart disease is substantially increased. In those with electrocardiographic left ventricular hypertrophy risk of cardiac failure is three times that in those with hypertension alone. Electrocardiographic left ventricular hypertrophy based solely on voltage criteria reflects chiefly the severity and duration of associated hypertension, carrying only half the cardiovascular risk of electrocardiographic left ventricular hypertrophy with repolarization abnormality. The precise pathologic and anatomic meaning of electrocardiographic left ventricular hypertrophy is unclear in view of the modest correlations with anatomic, x-ray, ventriculographic, and electrocardiographic measures of cardiac hypertrophy. The electrocardiographic aberrations are as much a product of myocardial damage as hypertrophy, and their appearance must be regarded as a grave prognostic sign in the course of cardiovascular disease.
Adult↗
[Ventricular arrhythmia in patients with hypertension and left ventricular hypertrophy].
Left ventricular hypertrophy is a problem in itself in patients with hypertension. Hypertensives with left ventricular hypertrophy have a higher incidence of ventricular arrhythmias and sudden death. This article reviews the epidemiological evidence in favour of this association. Although the mechanism of ventricular arrhythmias in patients with left ventricular hypertrophy in unclear, several hypotheses have been suggested including cellular electrophysiological changes, alterations of the myocardial tissue and silent myocardial ischemia. The management of ventricular arrhythmias in hypertensive patients implies an effort to prevent left ventricular hypertrophy by early and aggressive treatment and a judicious choice of antihypertensive agents capable of reducing left ventricular hypertrophy. It is also important to avoid hypokalemia and other electrolytic disorders. Antiarrhythmic drugs should be reserved for symptomatic patients who do not respond to other preventive measures.
Arrhythmias, Cardiac↗
[Advantages and disadvantages of ECG diagnosis in left ventricular hypertrophy].
Left ventricular hypertrophy (LVH) develops as a response to press or volume overload of the left ventricle. It is encountered in systemic hypertension, aortal stenosis and aortal insufficiency, mitral valve insufficiency, some congenital cardiac defects and hypertrophic obstructive cardiomyopathy. The most frequent cause of LVH in the adult population is hypertension. Prevalence of left ventricular hypertrophy in hypertensive individuals varies considerably, depending on the applied diagnostic method and characteristic of the group of hypertonic subjects. The presence of ECG signs of LVH is an infaust prognostic sign which at any level of blood pressure causes marked deterioration of the patient's prognosis. Classical ECG criteria for detection of LVH have a satisfactory specificity but low sensitivity. The sensitivity declines dramatically in the presence of obesity. The most sensitive but least specific criterium is high voltage in the precordial leads. The accuracy of ECG diagnosis of LVH improves considerably by multiplying the voltage by the duration of the QRS complex. Most probably the best results are obtained by Cornell's product. Falsely positive ECG signs of LVH (most frequently voltage criteria) are present in asthenic subjects. The author describes the case-history of a patient with hypertension who develops an ECG tracing imitating an infarction of the posterior wall and left ventricular hypertrophy with overburdening.
Diagnostic Errors↗
Mechanism of angiotensin II type 1 receptor blocker action in the regression of left ventricular hypertrophy.
Left ventricular hypertrophy refers to a pathologic increase in left ventricular mass and is associated with an increased risk of subsequent cardiovascular morbidity and mortality from any cause. In the development of left ventricular hypertrophy there is growth of cardiomyocytes and accumulation of extracellular matrix and fibrosis. The actions are partly induced by angiotensin II, the principal effector of the renin-angiotensin-aldosterone system, binding to the AT1 receptor. Biochemical markers, some implicated in inflammatory changes, correlate with changes in left ventricular mass. The reduction in left ventricular mass brought about with angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ARB) therapy correlates with a reduction in these inflammatory changes, monitored by brain natriuretic peptide. Recent studies incorporating trials of ARBs have found ARBs to be more effective in reducing left ventricular mass than beta blockers and possibly more effective than calcium antagonists. Initial studies suggest that ARBs and angiotensin-converting enzyme inhibitors may have similar effects in terms of reducing left ventricular hypertrophy, and the combination of angiotensin-converting enzyme inhibitors and ARBs is thought to be synergistic due to a more complete inhibition of the renin-angiotensin-aldosterone system. In conclusion, these agents are efficacious in antihypertensive therapy and can play an important role in the prevention or regression of left ventricular hypertrophy due to hypertension.
Angiotensin II Type 1 Receptor Blockers↗
[Heart failure in hypertensive patients with left ventricular hypertrophy].
Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Authors compared the presence of heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 192 hypertensives treated in our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 128 patients (mean age 65.9 years), absence of LVH in 64 patients (mean age 64.8 years). Both groups of hypertensives were matched by demographic parameters, by the presence of hyperlipidemia, by smoking habits. Hypertensive patients with left ventricular hypertrophy were more often treated by ACE inhibitors. There were statistically significant more patients with heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in LVH-positive patients than in LVH-negative once. There was also statistically significant lower ejection fraction (50.3 +/- 11.4% vs 56.5 +/- 7.4%) in LVH-positive patients than in LVH-negative once. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease with a high contribution to the development of chronic heart failure.
Adult↗
[QT dispersion intervals in hypertensives with left ventricular hypertrophy].
Left ventricular hypertrophy is an important risk factor of cardiovascular complications during the course of hypertension. Increased QT dispersion is associated with sudden cardiac death in congestive heart failure and in other cardiovascular diseases. Our aim was to compare QT dispersion from routine ECG in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Authors examined 71 hypertensives treated in our medical department. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. QT dispersion was defined from routine ECG (QTmax - QTmin). Presence of LVH was found in 26 patients (mean age 59.3 years), absence of LVH in 45 patients (mean age 57.8 years). Hypertensives with secondary hypertension, hypertrophic cardiomyopathy, sings of ischemia in ECG, arrhythmias, myocardial infarction, heart failure, diabetes mellitus and patients treated by antiarrhythmic drugs of the Ic and III groups were excluded. Both groups of hypertensives were matched by demographic parameters, and by the presence of hypertension, obesity, hyperlipidemia and smoking habites. There were statistically significant longer QT dispersion and QTc dispersion (59.0 +/- 20.1 ms, 64.0 +/- 23.7 ms) in LVH-positive patients than in LVH-negative once (43.2 +/- 9.5 ms, 48.4 +/- 11.1 ms). Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. Authors recommend to look after left ventricular hypertrophy presence in hypertensives as it carries much more complicated course of the disease. Measurment of QT dispersion adds farther stratificational information to these patients.
Adult↗
[Hereditary factors and left ventricular hypertrophy].
Left ventricular hypertrophy (LVH) is an independent risk factor for morbidity and mortality from cardiovascular disease in men and women with hypertension and in asymptomatic subjects with normal blood pressure. In hypertensive patients it is a stronger coronary risk factor than casual blood pressure readings. Correlation between levels of high blood pressure, duration of hypertension and left ventricular mass is poor. Epidemiological studies suggest that left ventricular hypertrophy may be influenced by genetic factors. In our review we present study groups of genes contributing to the development of left ventricular hypertrophy: 1) genes that encode components of hormonal pathways, 2) genes of key sympathetic and parasympathetic receptors, 3) genes that modify intracellular ion homeostasis, 4) genes that modify energy metabolism, 5) genes that modify motor unit composition and regulation. Angiotensinogen gene, angiotensin-converting enzyme gene, angiotensin receptor type 1 gene, aldosterone synthase gene, nitric oxide synthase gene, type A natriuretic peptide receptor gene, beta(2)-adrenergic receptor gene, G-protein beta(3) subunit gene are associated with left ventricular hypertrophy.
Angiotensinogen↗
Circadian blood pressure pattern in patients with treated hypertension and left ventricular hypertrophy.
Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P less than 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.
Antihypertensive Agents↗
[Antihypertensive treatment and left ventricular hypertrophy].
Left ventricular hypertrophy in arterial hypertension can be considered as an adaptive response of the heart to the increased afterload, in order to reduce wall stress; however, cardiac hypertrophy can also represent the first step toward a pathological process that leads to the development of congestive heart failure. Epidemiological studies have documented that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular morbidity and mortality. The possibility of reversing, or even preventing, left ventricular hypertrophy through a reduction in elevated blood pressure values and modification of some other pathogenetic factors should represent a major therapeutic need in the treatment of hypertensive patients. It has been demonstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because beyond control of blood pressure, the pharmacological interference with adrenergic system, the renin-angiotensin-aldosterone system or other growth factors can influence the development and the reduction of cardiac hypertrophy. Two recent meta-analyses of the principal regression studies have shown that ACE-inhibitors, followed by calcium antagonists and drugs capable of reducing sympathetic nervous system activity, are more effective in decreasing left ventricular mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated with an improvement of the functional consequences of an increased left ventricular mass. Further studies are needed in order to verify whether the reversal of left ventricular hypertrophy per se increases survival in essential hypertensive patients.
Adaptation, Physiological↗
QT-interval variability and autonomic control in hypertensive subjects with left ventricular hypertrophy.
Left ventricular hypertrophy is a risk factor for sudden death. Malignant ventricular arrhythmias originate from altered cardiac repolarization. Ample data have described spatial abnormalities in cardiac repolarization [QT interval (QT) dispersion] in subjects with hypertension; more data are needed on temporal changes. This study was designed to assess the QT variability index (QTVI), the slope between QT and the RR interval (QT-RR(slope)) and spectral QT variability in subjects with arterial hypertension. The results were compared with those from a population at high risk of sudden death, i.e. patients with hypertrophic cardiomyopathy (HCM) who had received an implantable cardioverter/defibrillator (ICD), and those from normotensive control subjects. A total of 44 hypertensive subjects, six patients with HCM and an ICD and 33 control subjects underwent simultaneous short-term recording (256 beats) of QT, RR and systolic blood pressure variability, in the supine position, during controlled breathing. QTVI and spectral components of QT variability in the hypertensive group were significantly higher than in normotensive control subjects (P<0.001), but significantly lower than in patients with HCM and an ICD (P<0.001). The severity of left ventricular hypertrophy correlated significantly with QTVI and the ratio of low-frequency (LF) to high-frequency (HF) power obtained from the RR variability spectra (RR(LF/HF), slope=0.24, P<0.05; QTVI, slope=4.06, P<0.0001; intercept, slope=2.40, P<0.05; chi(2)=38.8; P<0.0001). The QT--RR slope was significantly higher only in patients with HCM and an ICD (P<0.001). In conclusion, the increased QTVI and the correlation of this index with left ventricular hypertrophy indicates that hypertension increases temporal cardiac repolarization abnormalities. At the level of the cardiac sinus node, this alteration is associated with increased sympathetic and reduced vagal modulation. As already noted in patients with HCM, the increased QTVI could be a factor responsible for triggering malignant ventricular arrhythmias in subjects with hypertension.
Adult↗
[Evaluation of the cardiovascular risk in hypertensive patients: left ventricular hypertrophy].
Left ventricular hypertrophy is associated with a high risk of cardiovascular complications in all the populations in which it has been studied, especially in hypertensive patients. The echocardiographic measurements of left ventricular mass provides a quantitative approach to this risk, independent of the classical cardiovascular risk factors. It is very tempting to wish to replace the measurement of risk factors which, due to their great variability, are not easy to assess (blood pressure) by a marker which integrates several of them (blood pressure, age, weight, salt intake, blood viscosity, serum cholesterol ...) and their variation with respect to time. However, it is too early to recommend this practice for routine use. M mode echocardiographic measurement of left ventricular mass is relatively difficult technique feasible only in about 80% of the population. Even in the hands of experts, its reproducibility is far from perfect. Technical developments may lead to improvement. It remains to be demonstrated that the use of these values improves the management of hypertensive patients and this will not be an easy task. However the follow-up of left ventricular mass during treatment may be an alternative to trials of morbi-mortality in hypertensive patients with the advantage of requiring a shorter follow-up period and fewer patients. It also remains to be demonstrated that regression of left ventricular hypertrophy is accompanied by a corresponding reduction in cardiovascular complications.
Age Factors↗
Substrate metabolism, hormone interaction, and angiotensin-converting enzyme inhibitors in left ventricular hypertrophy.
Left ventricular hypertrophy is considered to be an independent risk factor giving rise to ischemia, arrhythmias, and left ventricular dysfunction. Slow movement of intracellular calcium contributes to the impaired contraction and relaxation function of hypertrophied myocardium. Myofibril content may also be shifted to fetal-type isoforms with decreased contraction and relaxation properties in left ventricular hypertrophy. Myocyte hypertrophy and interstitial fibrosis are regulated independently by mechanical and neurohumoral mechanisms. In severely hypertrophied myocardium, capillary density is reduced, the diffusion distance for oxygen, nutrients, and metabolites is increased, and the ratio of energy-production sites to energy-consumption sites is decreased. The metabolic state of severely hypertrophied myocardium is anaerobic, as indicated by the shift of lactate dehydrogenase marker enzymes. Therefore, the hypertrophied myocardium is more vulnerable to ischemic events. As a compensatory response to severe cardiac hypertrophy and congestive heart failure, the ADP/ATP carrier is activated and atrial natriuretic peptide is released to increase high-energy phosphate production and reduce cardiac energy consumption by vasodilation and sodium and fluid elimination. However, in severely hypertrophied and failing myocardium, vasoconstrictor and sodium- and fluid-retaining factors, such as the renin-angiotensin system, aldosterone, and sympathetic nerve activity, play an overwhelming role. Angiotensin-converting enzyme inhibitors (ACEIs) are able to prevent cardiac hypertrophy and improve cardiac function and metabolism. Under experimental conditions, these beneficial effects can be ascribed mainly to bradykinin potentiation, although a contribution of the ACEI-induced angiotensin II reduction cannot be excluded.
Adenosine Diphosphate↗