Maria T. Olivari

Nifedipine, a new antihypertensive with rapid action.

Oral (17 cases) or sublingual (9 cases) administration of nifedipine (10 mg), a new coronary dilator, induced a prompt and large pressure reduction in patients with severe primary hypertension. Pressure started to fall within 20 and 5 min after oral and sublingual administration, respectively, and reached the lowest levels in the next 10 min. Maximal mean arterial pressure reduction averaged 36 mm Hg; 120 min after the drug, mean arterial pressure was diminished by 19.5% of control. The hypotension was mediated through diminished peripheral resistance associated with rise of cardiac output and pulse rate. Nifedipine was also administered sublingually in 3 cases with hypertensive encephalopathy and acute left ventricular failure with average systemic and pulmonary arterial pressures from 307/164 and 91/55 mm Hg, respectively, which fell to 237/115 and 68/35 mm Hg 15 min after 10 mg of the drug, and were further reduced to 176189 and to 47/19 mm Hg by an additional 10 mg.

Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with ST segment depression and angina with ST segment elevation.

The function of both right and left sides of the heart was studied during spontaneous attacks of angina pectoris at rest in 7 patients showing ST depression (type I) and 4 showing ST elevation (type II) during the attack. In none of the 44 type I attacks and 29 type II attacks which were recorded did circulatory changes; the latter were different in the two groups. Type I attacks showed: a) a brief fall in arterial pressure, accompanied by b) a rise of right atrial and pulmonary wedge pressures and c) a decrease of cardiac output, right and left stroke work, the mean rate of systolic ejection, and indirect left ventricular pre-ejection dP/dt. In the course of the attack a hypertensive phase followed, which was paralleled by an increase of heart rate, cardiac output, left and right stroke work, and mean systolic ejection rate, left dP/dt; right atrial pressure and wedge pressure remained raised. All of the circulatory functions started to revert towards the pre-attack levels coincident with the waning phase of the electrocardiographic alteration, the latter occurring either spontaneously or after nitroglycerin. Type II attacks for the entire duration of the electrocardiographic changes showed: a) a reduction of arterial pressure, cardiac output, right and left stroke work, mean systolic ejection rate, and left dP/dt, b) a rise of right atrial and wedge pressures, and c) quite small changes of heart rate. When the electrocardiogram started to revert to the pre-attack aspect, the cardiac function rapidly improved and, after a supernormal phase, returned to the basal levels in about 2 minutes. It is concluded: 1) that no circulatory factor interfering with the mechanical effort of the heart is responsible for eliciting spontaneous angina: 2) that in type I attacks right and left ventricular impairment occurs which recovers rapidly, possibly through a sympathetic compensation; 3) that in type II attachs dysfunction of both sides of the heart occurs and persists throughout the episode of electrocardiographic alteration; 4) that the dynamic impairment is probably more severe in type I than in type II angina.

Pulmonary hemodynamics and right ventricular function in hypertension.

SUMMARYPulmonary and systemic hemodynamics in 16 hypertensive subjects (group I) with left ventricular (LV) hypertrophy (ECG and echo criteria) and in 17 hypertensive subjects with ECG signs of LV strain (group II), were compared with those in 14 normal individuals. An augmented pulmonary arteriolar resistance (PAR) in group I and to a larger extent in group II accounted for the pulmonary pressure elevation in both groups. Increase in PAR was unrelated to pulmonary blood flow and volume, pleural pressure, arterial PO2, PCO2 and pH, and could not be explained entirely by the left ventricular end-diastolic pressure changes.In group I, left (L.MSEJR) and right (R.MSEJR) mean systolic ejection rate, stroke index (SI) and mean velocity of circumferential fiber shortening (VCF) were enhanced in spite of the heightened pressure load on both sides of the heart. In group II, a large reduction of SI, L.MSEJR, R.MSEJR and VCF, as well as the relationship between ventricular filling pressures and SI, documented a compromised performance of both ventricles.Findings indicate that: systemic hypertension is associated with elevation of pulmonary arterial pressure and of PAR which is not necessarily a consequence of impairment in LV function; LV hypertrophy is associated with enhanced performance of either ventricle; in coincidence with development of ECG signs of LV strain, the performance of both sides of the heart deteriorates.A functional interdependence of the two ventricles is suggested.

Cardiac load and function in hypertension: Ultrasonic and hemodynamic study

On the basis of echocardiographic measurements, 46 patients with established, uncomplicated primary hypertension (diastolic pressure = 100 mm Hg) were classified as: those with a normal-sized heart (Group I, 13 patients); those with left ventricular concentric hypertrophy (Group II, 19 patients); and those with left ventricular hypertrophy and enlargement (Group III, 14 patients). Eighteen age-matched healthy subjects were investigated as the controls. The function of both the left and right ventricle, evaluated by the stroke index-filling pressure relation and by the mean rate of ejection, was maintained in Group I, augmented in Group II and reduced in Group III, in comparison with the controls. Left ventricular mean rate of circumferential fiber shortening (Vcf) was normal in Group I, significantly augmented in Group II and definitely reduced in Group III. It could not be established whether the divergent variation from normal of the Vcf in Groups II and III reflected opposite changes in ventricular contractility or in afterload (wall stress during ejection), or both. However, the parallel functional pattern of the right and left ventricle in these two groups suggests a functional interdependence of the two sides which cannot be interpreted in terms of afterload but is best explained by changes in the contractile state of the whole heart.

Repetitive myocardial ischemia of Prinzmetal type without angina pectoris.

In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetals angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetals angina can occur even in the absence of angina pectoris.

Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal.

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.

Antihypertensive action of propranolol in man: lack of evidence for a neural depressive effect.

The hypothesis that a neural depressive action is related to the antihypertensive effects of beta blockers has been evaluated in 14 essential hypertensive male patients through the circulatory response to noxious stimuli. The pressor reaction to mental arithmetic was primarily mediated by cardiac stimulation (beta receptors activation), that to cold by vasoconstriction (alpha receptors activation). Arithmetic and cold were tested to separate the effects of peripheral beta blackade from possible neural and other influences. After propanolol (320 mg per day for 3 wk): (1) The baseline pressure was reduced; (2) appearance, peak, and disappearance time of the circulatory reaction to either stimulus was not altered; (3) the pressor e.ffect of arithmetic was decreased in an extent proportional to the reduced rise of cardiac output; and (4) pressure during cold reached the pretreatment levels through an augmented increase of vascular resistance. Our findings indicate that propranolol depresses only the circulatory reactions mediated through beta receptors activation and provide no evidence of effects other than beta blockade.

Influences of the adrenergic nervous system on the repolarization phase of the electrocardiogram.

The following conclusions can be drawn : (1) The nervous outflow to the heart may be varied from the baseline to opposite directions by different stressful stimuli. (2) ST-T alterations may be induced and abolished by adrenergic activation and inhibition respectively. (3) These effects are dissociated from or not necessarily associated with an exaggerated responsiveness of the cardiac beta receptors. (4) The adrenergic influences on the ST-T abnormalities of myocardial ischemia and hypertension are limited.

Cardiac performance in hypertension re-evaluated through a combined haemodynamic ultrasonic method.

From echocardiographic measurements, 39 patients with established, uncomplicated primary hypertension (diastolic pressure > 100 mmHg) were classified as follows: normal-sized heart (group 1, 10 cases); concentric left ventricular hypertrophy (group 2, 18 cases); left ventricular hypertrophy and cavity enlargement (group 3, 11 cases). Eighteen age-matched healthy subjects were investigated as a control group. Systolic and diastolic arterial pressure increased progressively from group 1 to 2 to 3. Left ventricular function, assessed from the relation between diastolic diameter and stroke index, was maintained in group 1, increased in group 2 (in spite of the greater pressure load), and reduced in group 3, in comparison with controls. Similarly, the mean velocity of circumferential fibre shortening (VCF) was normal in group 1, significantly increased in group 2, and reduced in group 3. It was impossible to discern whether the different behaviour of VCF in group 2 and in group 3 reflected opposite changes in ventricular contractility, or in wall stress during ejection, or in both. At variance with previous conclusions (which were based on utilisation of electrocardiographic and chest x-ray criteria to define hypertrophy) it is suggested that left ventricular concentric hypertrophy in man consequent to sustained hypertension is associated with an improved function. Whether this feature depends upon an augmented contractility or a ventricular unloading effect related to hypertrophy remains uncertain.

Echocardiographic and hemodynamic correlates in Prinzmetal angina pectoris: A case report

In a patient suffering from Prinzmetal angina pectoris, ischemic attacks of the anterior left ventricular wall were associated with the following changes: fall in cardiac output; increased left ventricular diastolic pressure (LVDP) and volume; flattening of the septal motion; marked reduction of the mitral valve early diastolic amplitude and rate of opening; and marked reduction of the systolic closure velocity. It is suggested that LVDP rise depends, at least in part, on variations in left ventricular diastolic volume and segmental wall motion, and that disruption of the mitral valve motion derives from changes in LVDP and flow through the mitral orifice.