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Arterial hypertension (AH) is one of the basic components of metabolic syndrome that is caused by four factors: autonomic sympathetic dysfunction; activation of the hypothalamic-pituitary-adrenal axis; that of the renin-angiotensin-aldosterone system; and endothelial dysfunction (ED). AH is a slowly progressive hemodynamic disease, the natural course of which is characterized by not only elevated blood pressure (BP), but also by left ventricular hypertrophy, arterial remodeling, and a progressive increase in total peripheral resistance. ED and arterial remodeling play a key role in the pathogenesis of AH in metabolic syndrome. Remodeling of resistant arteries raises peripheral resistance and stabilizes BP and that of large arteries increases their stiffness and a reflected wave, resulting in increased pulse BP, systolic BP, and enhanced left ventricular hypertrophy. Insulin resistance and hyperinsulinemia increase the activity of the renin-angiotensin-aldosterone system and, by enhancing the expression of angiotensinogen, angiotensin II and its type 1 receptors, favors the development of AH, proinflammation, atherosclerosis, and congestive heart failure. Hyperleptinemia, which, by stimulating the activity of the sympathetic nervous system, elevates BP, plays a certain role in the development of AH in metabolic syndrome and obesity.

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Psychosomatic status was investigated in 104 patients with essential hypertension (EH) and 111 patients with secondary arterial hypertension (AH) of renal origin in the presence of chronic pyelonephritis. A significant heterogeneity of psychological characteristics was established in patients with these two clinical forms of AH. In EH patients psychological deviations were detected since very early stages of the disease, but they did not become more profound with stabilisation of blood pressure. At the same time the progress of secondary AH was accompanied by obvious deterioration of initially little-changed psychological status, which correlated with the gravity of somatic status, in particular, with the severity of left ventricular hypertrophy.

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Altogether 58 patients suffering from arterial hypertension (AH) were examined. The patients with left ventricular hypertrophy (LVH) and changes in the ST-T demonstrated a high correlation between an increase of the end systolic tension (EST) and interval elongation and the minimal size of the left ventricle before mitral valve opening. These data point to the development of "high-stressful LVH" which is accompanied by a non-proportional increase of EST, subendocardial ischemia of the myocardium (changes in the ST-T) and derangement of diastolic heart function.

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One hundred and forty-seven patients with essential hypertension (EH) and 126 patients with secondary arterial hypertension (AH) on the basis of chronic pyelonephritis were studied by means of radiocardiography with 131I-albumin and M-mode echocardiography. The importance of the haemodynamic type of circulation for the development of left ventricular hypertrophy (LVH) was established. Correlative analysis revealed that the influence of arterial pressure (AP) on LVH is increased by stabilization of AH, especially in patients with the normo- and hypokinetic types of circulation; interestingly, the relation between LVH and systolic pressure was closer than that between LVH and diastolic pressure, especially in patients with secondary AH. Moreover, it was shown that the development of LVH is due to a preferential increase in posterior wall thickness in essential hypertensives and in ventricular septal thickness in secondary hypertensives, although all patients with LVH had dilatation of the left ventricular cavity.

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Seventy eight patients with arterial hypertension were examined by echo-, radiocardiography and scintigraphy of the myocardium, using 99mTc pyrophosphate and 201Tl. A relationship was found between the development of hypertrophy of the left ventricle and the impairment of it perfusion and function. At the same time there was a correlation between the decrease in cardiac output and the deterioration of myocardial blood supply. It was demonstrated that 99mTc pyrophosphate or 201Tl myocardial scintigraphy yielded the coincident results when relative heart failure was evaluated in patients with arterial hypertension and left ventricular hypertrophy.

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Intravenous verapamil infusion reduced the arterial pressure (AP) in 13 out of 71 (76.5%) patients with severe arterial hypertension (AH) refractory to a two-week, three-step oral antihypertensive medication. Investigations including echo- and radio-cardiography were performed: in the control period before starting the three-step treatment; after two weeks before intravenous verapamil infusions; 10 days after stopping the verapamil administration, and before leaving the hospital during continued 3-4 weeks three-step therapy. The AP reduction was caused by decreased total peripheral resistance. Verapamil administration improved also intracardiac haemodynamics and left ventricular contraction. The AP was effectively controlled even after stopping the verapamil administration and continuing the three-step oral antihypertensive treatment. No manifest changes in the left ventricular function were registered.

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A study was undertaken to examine 285 patients with hypertensive disease and 187 with secondary arterial hypertension. Their hemodynamic parameters were assessed by a radionuclide method. It was found that there were various blood circulatory types at each stage, no matter what the clinical type of the disease. The state of central hemodynamics was demonstrated to be associated with interaction of cardiac and peripheral mechanisms responsible for blood circulatory regulation.

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As many as 75 patients with essential hypertension were examined by echocardiography and radiocardiography. The development of hypertrophy was accompanied by the rise of the diastolic dimensions of the left ventricle regardless of the type of the heart overload (by volume or pressure). As left ventricle hypertrophy developed, the myocardial contractility declined and normal hemodynamic function of the heart was maintained due to the Frank-Starling mechanism. The relationship has been established between the intensity of hypertrophy, left ventricle function and the hemodynamic profile of the disease.

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A study of 32 patients with arterial hypertension using echocardiography, electrocardiography and myocardial 99mTc-pyrophosphate scintigraphy, demonstrated that developing left-ventricular hypertrophy may interfere with myocardial perfusion. Regression of left-ventricular hypertrophy and recovery of myocardial perfusion is shown to be possible under the effect of antihypertensive treatment.

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The authors presented the results of a combined radionuclide study of the state of pulmonary hemodynamics in patients with essential hypertension. Altogether 132 patients were investigated. Radiocardiography, perfusion scintigraphy and a study of the regional pulmonary blood flow using radioactive Xe were conducted. An analysis of the results has shown that in some patients pulmonary hypertension develops even at early stages of the disease and is particularly marked in stages IIB-III. The mechanism of development of pulmonary hypertension depended at each stage on the interrelationship and time course of indices that characterized pulmonary circulation, and was of different nature. Hemodynamic disorder was manifested in blood mass redistribution from the lower lung regions to the upper ones, slowing down of rate parameters and a raise of pulmonary vascular resistance.

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Dispensary care was provided to 122 patients with essential hypertension. During a 3-year follow-up period BP decrease in regularly treated patients (44) was accompanied by the restoration of hemodynamic cardiac function and regression of myocardial hypertrophy and ischemia. BP stabilization, transformation of the blood circulation of hemodynamic type, an increased degree of myocardial hypertrophy and ischemia were noted in irregularly treated patients.

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Disorders of left-ventricular diastolic relaxation and blood filling in patients with first- and second-stage essential hypertension are shown, by means of echo-, radio- and apexcardiography, to be due to the effects of arterial blood pressure, hemodynamic changes, heart rate and the magnitude of left-ventricular hypertrophy. Antihypertensive treatment, affecting major parameters of disease, brings about the recovery of the heart's diastolic function.

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The effects of short-term antihypertensive therapy were assessed using echo- and electrocardiography, in patients with first- or second-stage essential hypertension, with respect to possible reverse development of left-ventricular hypertrophy and myocardial ischemia. A reduction of left-ventricular hypertrophy was found to be possible, with regard to the hemodynamic type, in patients with mild or moderate essential hypertension provided their blood pressure was controlled effectively. Reverse development of electrocardiographic signs of myocardial ischemia (ST segment and T wave reaching their normal values) is possible through a decrease of arterial BP and a reduction of adrenergic effects on the heart.

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The antihypertensive effect of finoptin (verapamil) and corinfar (nifedipin) and their impact on the hemodynamics and the repolarization complex of the ECG were studied in 52 patients with essential hypertension and 48 patients with secondary arterial hypertension. The calcium antagonists were found to effectively decrease the blood pressure by reducing the peripheral resistance. Verapamil may be recommended for the monotherapy of mild and moderate forms of arterial hypertension, whereas corinfar should be used in cases of marked hypertension and at the third stage of therapy. Patients with electrocardiographic signs of myocardial ischemia show the normalization of the ST segment and a decreased depression of T wave under the impact of corinfar.

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A total of 120 patients with essential hypertension, stage I and II, were examined, using radio- and electrocardiography, before and after a hypotensive treatment. Two mechanisms: excessive volume (in patients with hyperkinetic circulation) and excessive pressure (in those with normo- and hypokinetic circulation) were found to form the basis of the formation of left-ventricular muscular hypertrophy. Antihypertensive effect of treatment reducing electrocardiographic signs of left-ventricular muscular hypertrophy was shown to be related to improved arterial pressure control and lesser adrenergic influence on the heart.

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