Intermittent high altitude hypoxia.

The effect of intermittent high altitude (IHA) hypoxia on the myocardium and lesser circulation was investigated in adult male Wistar rats. IHA can induce intermittent pulmonary hypertension and right ventricular hypertrophy in a relatively short time. Even marked pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular changes can be normalized when rats are removed from the hypoxic atmosphere. At the beginning of the exposure to IHA acute myocardial necrotic changes were found; prolongation of IHA did not lead to further acute lesions. Experimentally induced CO polycythemia leads to mild pulmonary hypertension; IHA-induced pulmonary hypertension may, thus, be partly due to polycythemia. Beta blocking agents are able to decrease chronic hypoxic pulmonary hypertension, hypertensive changes in the pulmonary circulation, the degree of right ventricular hypertrophy, and necrotic myocardial changes.

Echocardiographic assessment of the left ventricle in juvenile hypertension.

We studied with M-mode echocardiography the morphology and function of the left ventricle in a group of 36 juvenile hypertensives with borderline hypertension, whose cuff arm pressure exceeded 150/90 mmHg in at least three separate sessions. The results were compared with those of 23 age-matched normotensives with no evidence of any cardiovascular disease. Left ventricular hypertrophy (i.e. septum and/or posterior wall thicknesses in diastole greater than or equal to 12 mm) was present in 13 subjects of the hypertensive group (36%). Significant increase of interventricular septal thickness together with higher septum/posterior wall ratio and a higher incidence of asymmetric septal hypertrophy were the most characteristic findings in juvenile hypertensives. Of the functional parameters the only observed difference between the two groups was an elevated peak velocity of left ventricular contraction in hypertensives which tended to correlate inversely with the values of septum/posterior wall ratio. Additional comparison of electrocardiographic and echocardiographic detection of left ventricular hypertrophy in young hypertensives revealed a lower sensitivity but a satisfactory specificity of electrocardiography (31 and 87% respectively). The results indicate that besides an elevated systemic arterial pressure, other factors such as increased sympathetic or humoral activity may play a role in the incipient stage of essential hypertension and that isolated septal hypertrophy seems to be an early sign of cardiac involvement.

Haemodynamic effects of physical training in essential hypertension.

The haemodynamic effects of four weeks of daily intensive training on bicycle ergometer were studied in 10 men with essential hypertension of grade II (WHO). Three weeks before training all medication was replaced by placebo. Five days before onset of training all patients underwent a haemodynamic examination using floating catheter and direct brachial arterial pressure at rest and during effort. The same examination was repeated within five days after the completion of the training. Resting measurements did not demonstrate any effect of the training on systemic pressure or central haemodynamics. At the given load, however, a significant decrease for the pressor response occurred, i.e. lowering of systolic, mean and diastolic arterial pressure. Peripheral vascular resistance was not affected. Cardiac output (Fick) decreased insignificantly both at rest and during effort after training. Heart rate decreased significantly only during exercise. The training lowered significantly both tension time index and left ventricular stroke work index. No adverse clinical or haemodynamic effects of short intensive training were detected in hypertensive patients. There was no evidence of changes in pulmonary artery diastolic pressure considered as an indicator of the left ventricular filling pressure. The heart volume remained unchanged after training.