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Biomedical subjects

M Guazzi

Publications and source records attributed to M Guazzi.

At least 127 records · Page 7Linked to original sources
PubMed1976

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 effect 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.

Adrenergic beta-Antagonists↗
PubMed1976

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 Prinzmetal's 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 Prinzmetal's angina can occur even in the absence of angina pectoris.

Angina Pectoris↗
PubMed1976

Cardiac function in the treatment of arterial hypertension with propranolol.

1. Propranolol, when used for treating arterial hypertension, may influence determinants of both cardiac and vascular function; the consequent changes in cardiac performance may result from the interaction of different and possibly opposite effects. 2. Cardiac funtion was investigated in fifty-four primary hypertensive men in the pretreatment state and after 3 weeks of propranolol therapy at a daily dose of 320 mg. 3. beta-Receptor blockade caused depression of pre-injection left ventricular function, which was unrelated to the direction and the extent of changes in peripheral circulation. 4. The ejection left ventricular function could be either depressed or improved depending on the direction to which treatment shifted the vascular resistance, and consequently, the impedance to left ventricular ejection. 5. Withdrawal of the adrenergic support is probably the major factor responsible for the poor ventricular adaptation to an augmented impedance.

Cardiac Output↗
PubMed1975

Negative influences of ascites on the cardiac function of cirrhotic patients.

Right and left ventricular function was evaluated in 21 men with cirrhosis and tense ascites during staged removal of ascitic fluid. During paracentesis it was observed (1) that there was a significant increase in cardiac output, stroke volume, right and left ventricular stroke work and mean rate of systolic ejection; (2) that up to a certain stage of drainage (about 5,000 ml), there was a relationship between the amount of fluid removed and the intraabdominal and right atrial pressures and (3) that there was a direct relationship between improvement of cardiac function and normalization of right atrial pressure. It is believed that the increased intra-abdominal hydrostatic pressure acting upon the diaphragm affects the intrathoracic pressure to such an extent that the transmural filling pressure of the heart is reduced, and the mean pressure and respiratory pulsations of the right atrium increased, all of which impede venous return. Improved cardiac function during paracentesis appears to be due to an augmented filling of the heart and to a larger venous return.

Adult↗
PubMed1975

Electrical and dynamic responses of the human hyperkinetic heart to sympathetic stimuli.

1. The elevated beta-receptor responsiveness to adrenergic stimuli makes subjects with the primary hyperkinetic cardiac syndrome ideal for studying the electrical and dynamic responses of the heart to sympathetic activation. 2. In twelve men presenting with the syndrome, the effects of mental arithmetic and painful (cold) stress on the cardiac inotropic state were tested and correlated with the concomitant electrocardiographic changes. 3. Arithmetic and cold evoked responses opposite and divergent from the base-line state: the former induced vasodilatation, enhancement of cardiac rate, output, contractility and deep T wave inversion; the latter caused vasoconstriction, cardiac depression and full restoration of repolarization. 4. The sympathetic outflow elicited by stress is not generalized, but selectively directed to different circulatory levels in relation to the stimulus at work; cardiac sympathetic stimulation or inhibition has opposite effects on the repolarization phase.

Adolescent↗
PubMed1975

Stress-induced and sympathetically-mediated electrocardiographic and circulatory variations in the primary hyperkinetic heart syndrome.

As shown by the inotropic changes, the sympathetic discharge on the heart, is selectit syndrome. In the steady state the electrocardiogram shows flat, diphasic, or "tucked' T waves. Mental stimulation or isoproterenol, and, respectively, pain or beta blockade induce changes of the repolarization phase divergent from steady state. The former causes ST depression and deep T-wave inversion and the latter fully normalizes the repolarization phase. It is concluded that the electrical activity of the heart is directly influenced by the adrenergic drive in this disorder, and that different stressful factors can alter the repolarization phase in opposite ways in relation to the influence of the stimulus on the cardiac sympathetic tone.

Adolescent↗
PubMed1975

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.

Angina Pectoris↗
PubMed1975

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.

Angina Pectoris↗