Is left ventricular hypertrophy a risk factor in hypertensive patients?

BACKGROUND: Left ventricular hypertrophy (LVH) is supposed to be a risk factor of cardiovascular (CV) complications in hypertensive patients. AIM: To compare clinical events in hypertensives with and without LVH. PATIENTS AND METHODS: 319 hypertensives with LVH (mean age 64.1+/-10.6 ys) and 177 hypertensives without LVH (mean age 62.5+/-11.3 ys). LVH defined by echo Penn convention as left ventricular mass index >134 g/m2 in men and >110 g/m2 in women. Clinical events--heart failure (EF<40 %), left ventricular diastolic dysfunction (echo-doppler: transmitral-flow where peak A>peak E), myocardial infarction (history, ECG, cardiac enzymes), chronic atrial fibrillation (more than 2 weeks duration), mitral regurgitation (echo) and renal involvement (creatininemia>120 micromol/l). The two groups of hypertensives were matched by demographic criteria, duration and intensity of hypertension, obesity, diabetes mellitus, lipid serum levels and smoking habits. RESULTS: There were statistically significant at least p<0.05 more CV events (heart failure, left ventricular diastolic dysfunction, myocardial infarction, chronic atrial fibrillation, and mitral regurgitation cases) and renal involvement in LVH-positive patients than in LVH-negative patients. CONCLUSION: LVH is a strong risk factor for clinical events in hypertensives, which necessitates their more intensive treatment, mainly with drugs producing also LVH regression. (Tab. 5, Ref. 48.)

[The role of infection and inflammation in the pathogenesis of atherosclerosis]. / Uloha infekcie a zápalu v patogenéze aterosklerózy.

Pathogenesis of the atherosclerotic process is deemed as multifactorial. To the most important risk factors, besides certain family predisposition, there belongs hypercholesterolemia, arterial hypertension, obesity, diabetes mellitus, smoking and others. In the last years there are more and more data about the role of inflammation and infection in the whole development of atherosclerosis. The witness for this hypothesis is the findings of high parameters of inflammation in involved vessels as well as in the blood of atherosclerosis suffering persons. Opinions about the inflammation theory appear from the 90th. Local sterile inflammation in the subendotelium of the middle and big arteries has been proved to consist of specific immune reaction (activation of the T-lymphocytes) as well as nonspecific characteristic by elevated monocytes in the artery wall during the whole process of atherogenesis. Inflammation in the plaque can trigger and hold several factors engaged in the atherosclerotic process, such as oxidized LDL cholesterol, elevated production of various superoxides, activated macrophages, activated T-lymphocytes, cytokines (IL-1, IL-6, interferon gamma) and lipoprotein Lp (a). In this inflammation process levels of CRP (acute phase protein), fibrinogen and erythrocyte sedimentation are elevated as a reaction of the organism to nonspecific chronic infections. Because of this it is thought that elevated fibrinogen and erythrocyte sedimentation are markers of the cardiovascular risk. Some papers deal with antiinflammatory effects of statins, because these lower CRP levels so they also lower atherosclerotic risk through not only lowering of cholesterol levels. Also asprine, as an antiinflammation agent, changing the CRP levels, would be of benefit for patients with vascular disease because its antiaggregation and antiinflammatory effects. ACE inhibitors are also antiinflamatory through blocking of tissue production of angiotensin II (artery wall and atherosclerotic plaque). Enzymatic inhibitors changing angiotensin can also have a partial antiinflammatory effect. The infection theory is supported also by tracing of some microorganisms in the atherosclerotic plaque or in the blood, as e.g. Helicobacter pylori or Chlamydia pneumoniae; to the autoimmune origin is indicated the presence of the specific immunity reaction against heat shock proteins (HSP) or oxidized LDL. This infection theory offers new therapy possibilities. Therefore eradication for example by antibiotics can lead to stabilization of the atherosclerotic plaque with positive consequences, as it was discovered by many studies.

[Heart failure in hypertensive patients with left ventricular hypertrophy]. / Srdcové zlyhanie u hypertonikov s hypertrofiou l'avej komory.

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.

Relation of left ventricular hypertrophy to cardiovascular complications in diabetic hypertensives.

The presence of diabetes mellitus and other risk factors of atherosclerosis, such as obesity, smoking and hyperlipidemia, in hypertensive patients makes the prognosis worse. Authors compared the clinical findings in diabetic hypertensive patients with and without left ventricular hypertrophy, the presence of which was diagnosed and defined by echocardiography. The study is based on the analysis of hospital records of 115 hypertensive patients treated at our department during the period 1998-1999. Left ventricular hypertrophy (LVH) was defined by echocardiography as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Left ventricular hypertrophy was found in 79 patients (mean age 64.6 ys) but not in 36 patients (mean age 63.3 ys). Both groups were matched as to age and sex, intensity and duration of hypertension and diabetes, obesity, smoking and hyperlipidemia. In LVH-positive patients, there was a statistically significant incidence of heart failure, mitral regurgitation and renal involvement and a more non-significant incidence of left ventricular diastolic dysfunction, myocardial infarction, chronic atrial fibrillation and stroke than in LVH-negative ones. Left ventricular hypertrophy usually complicates the course of hypertension. Authors recommend to investigate the presence of left ventricular hypertrophy in hypertensives as it carries a much more complicated course of the disease. (Tab. 5, Ref. 28.)

[QT dispersion intervals in hypertensives with left ventricular hypertrophy]. / Disperzia QT intervalov u hypertonikov s hypertrofiou l'avej komory.

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.

[Left ventricular hypertrophy in hypertension]. / Hypertrofia l'avej komory u hypertonikov.

Left ventricular hypertrophy LVH is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Occurrence of other risk factors of atherosclerosis in these hypertensive patients such as hyperlipidemia and smoking deteriorate the prognosis too. The authors compared clinical findings in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 185 hypertensive patients treated at 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 109 patients (mean age 66.7 years), absence of LVH in 76 patients (mean age 64.7 years). Both groups of hypertensive patients were matched by demographic parameters by the presence of hyperlipidemia and by smoking habits. Hypertensive patients with diabetes mellitus and obesity were excluded. They were statistically significant in the incidence of heart failure, myocardial infarction, renal failure and mitral regurgitation, and non-significant in the incidence of left ventricular diastolic dysfunction. There were more cardiovascular complications in LVH-positive patients than in those with LVH-negative findings. The incidence of stroke was slightly higher in LVH-negative patients. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. The authors recommend to examine the patients with arterial hypertension for the presence of left ventricular hypertrophy as it complicates the course of the disease significantly. (Tab. 3, Fig. 2, Ref. 26.)

[Hypertrophy of the left ventricle--etiopathogenesis, clinical consequences and prognosis]. / Hypertrofia lavej komory--etiopatogenéza, klinické dôsledky a prognóza.

The left ventricular hypertrophy is a risk marker of the cardiovascular morbidity and mortality in hypertensive patients--it contributes to sudden death, myocardial infarction, myocardial ischemia, heart failure, arrhythmias, left ventricular diastolic dysfunction, stroke and renal failure. The mechanisms by which the heart hypertrophy increases the risk of cardiovascular morbidity and mortality, however, is not completely clear yet. Pressure overload (resulting in the concentric hypertrophy) and volume overload (resulting in the eccentric hypertrophy) of the left ventricle play a significant role in the development of the hypertrophy of the left ventricle. Other risk factors, stimulating left ventricular hypertrophy, include growth factors, genetic predisposition, age, obesity, hyperinsulinemia and anemia. The hypertrophy of left ventricle most often occurs with hypertension, cardiomyopathy and aortic stenosis. Several clinical studies evaluated functional consequences of the reduction of the ventricular hypertrophy and found out that the function of the left ventricle to be improved in hypertensive patients who had undergone an effective and long-term antihypertensive treatment. However, these studies did not differentiate whether for the improvement in the function of left ventricle was the matter of the reduction of the left ventricular mass or whether it was because of the decrease of the arterial pressure during the period of anti-hypertensive treatment. On the basis of the literature studied we can emphasize that the reduction of myocardial hypertrophy resulting from a specific antihypertensive treatment appears to be more favourable than harmful for the heart's pump performance.