[Effects of coenzyme Q10 on the contractility and fibrillation threshold of isolated rabbit heart during ischemia and reperfusion].
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Biomedical subjects
Publications and source records attributed to B Magnani.
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The effect of intravenous enoximone on forearm venous circulation was studied in ten healthy volunteers (group A) and in ten patients with NYHA class III-IV congestive heart failure (group B). Distensibility of the forearm capacitance vessels was assessed from pressure-volume curves by venous occlusion plethysmography using a mercury-in-rubber strain gauge. Three recordings each at 3-min intervals were obtained before the infusion and again 20 min after completion of the infusion. Venous volume changes (VV) at congesting pressures of 10, 20, and 30 mmHg before and after enoximone were compared. Forearm muscle blood flow was also measured by venous occlusion plethysmography; electrocardiogram, heart rate, and cuff blood pressure were recorded throughout. Enoximone at a dose of 1 mg/kg body weight was infused over 10 min through a peripheral vein in group A and via a central line in group B. In group A, the effect of the injection vehicle was also assessed. VV10, VV20, and VV30 did not differ from baseline values after enoximone in both groups A and B. The vehicle caused a small but significant degree of venoconstriction in group A (VV20, 2.64 +/- 0.9 to 2.48 +/- 0.83 ml/100 ml, P less than 0.05; VV30, 3.47 +/- 1.27 to 3.33 +/- 1.20 ml/100 ml, P less than 0.05), which could be explained by an acute response to local pain from the infusion. This effect was not evident following enoximone, perhaps as a result of its counterbalancing vasodilating action to venoconstriction induced by acute pain.(ABSTRACT TRUNCATED AT 250 WORDS)
The hemodynamic effects of increasing dosages of felodipine, a new calcium antagonist with selective vasodilator properties, were studied in 13 patients with chronic cardiac failure. A Swan-Ganz thermodilution catheter was positioned in the pulmonary artery and hemodynamic parameters were monitored from 9 am to 6 pm for five days. On the first and the fifth day patients received placebo (P) and on the second, third, and fourth day patients received felodipine 5, 10, and 20 mg, respectively. Symptom-limited exercise tests with a bicycle ergometer were performed on both days of P and on the fourth day. A marked reduction of systemic vascular resistance (SVR) and a significant increase of cardiac index without increments of heart rate (HR) were observed after felodipine at rest. A dose response effect could be demonstrated. During exercise a significant increment of cardiac index and decrease of pulmonary wedge pressure was observed after felodipine. Felodipine showed a potent vasodilator action on systemic circulation with significant changes on both stroke volume and filling pressures at rest and during exercise without side effects.
The effects of coronary artery revascularization and perioperative myocardial infarction on left ventricular wall motion are still controversial. In this study perioperative myocardial infarction was quantitatively estimated with the cumulative activity of the CK-MB isoenzyme in the perioperative period in a group of 77 consecutive patients undergoing coronary artery bypass surgery. After the operation (on average 9 +/- 1.8 months) all the patients were submitted to left ventricular and coronary angiography. Overall the global left ventricular ejection fraction was unchanged after the operation. The subgroup of patients with all patent grafts showed an improvement of both regional wall motion (P less than 0.05) and ejection fraction (from 58 +/- 13 to 64 +/- 13%, P less than 0.005); the number of angiographically abnormal left ventricular segments decreased from 28.5 to 16.6% (P less than 0.001). The cumulative activity of CK-MB enzyme was significantly correlated with the pre- and postoperative changes of ejection fraction (r = -0.51, P less than 0.01). Thus coronary artery bypass surgery can improve regional wall motion, but the likely benefit is observed in the absence of a perioperative myocardial ischemic damage.
Among the various treatments adopted to protect the acutely ischaemic myocardium, favourable results have been reported for beta-blockers. Nitrates can also reasonably be expected to exert favourable effects in acute myocardial infarction considering their haemodynamic action. In this study we compared the haemodynamic effect of metoprolol alone with the effect of metoprolol plus nitroglycerin. Fourteen patients, admitted within 12 hours from the clinical onset of acute myocardial infarction, were initially given intravenous metoprolol (5 + 5 + 5 mg) followed 15 minutes later by an additional 50 mg oral dose. Thereafter, they were randomly allocated to a treatment with metoprolol alone (Group 1) or metoprolol plus intravenous nitroglycerin (Group 2). The two groups were comparable with regard to age, sex, time to admission, time to therapy, site of necrosis, Killip class, and infarct size. Acute beta-blockade induced a marked decrease of cardiac output, systolic blood pressure and heart rate along with a small increase of pulmonary wedge pressure and a marked systemic vasoconstriction. In Group 1 patients these haemodynamic changes persisted up to twelve hours after randomization; in Group 2 patients the addition of nitroglycerin induced a prompt decrease of pulmonary wedge pressure and peripheral vascular resistance whereas the double product was unchanged. In conclusion, intravenous nitroglycerin induces a beneficial haemodynamic effect after early beta-blockade with metoprolol.
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The efficacy of intravenous propafenone (P) infused at 2 mg/kg in 3 min as a loading dose followed by 0.007 mg/kg/min along 24 hours, in converting atrial fibrillation (AF) was evaluated under continuous electrocardiographic and blood pressure control in 22 patients. In case of inefficacy after a wash out of 24 hours, amiodarone (A) 5 mg/kg in 3 min followed by 1.8 gr/24 hours was infused. AF had to be constant (at least one 24/hour Holter recording) and of recent onset. All the patients were NYHA class 1 or 2. Ten patients reverted to sinus rhythm after P usually within 60 min; two of the non responders reverted after A and ten did not revert at all. RR intervals were significantly shorter in the responders compared to the others: mean value 537 +/- 64 vs 771 +/- 200 msec (p less than 0.001). During P the QRS duration increased 12.9% (p less than 0.005) and QTc of a lesser extent 7.8%; during A QRS did not modify significantly and QTc prolonged 9.5% (p less than 0.002). Propafenone i.v. infusion appears to be a rapid effective method of converting recent onset AF to sinus rhythm in patients with high ventricular rate. Amiodarone i.v. does not significantly help in converting to sinus rhythm the patients non responder to P.
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An electrophysiologic study (EPS) has been performed before and after cardioplegia in 50 patients (pts) who underwent a coronary by-pass graft intervention (CBPG) in order to investigate the possible mechanism explaining the frequent episodes of paroxysmal atrial fibrillation (PAF) complicating the early follow-up and the possible role of the type of caval cannulation. Twenty-five pts underwent a separate caval cannulation and twenty-five only cannulation of the inferior vena cava. EPS has been performed before (34 degrees C) and after cardioplegia (37 degrees C). PAF complicated the 15 days early follow-up of 32% of the pts; 24% of the pts operated with 1 cannula and 40% of the operated with 2 cannulae respectively (N.S.). The pts with AF had an high percentage of splitting of the atrial signals during atrial premature stimulation (77% vs 5%, p less than 0.002) and a significant dispersion of the conduction times between high and low right atrium (36 +/- 21 vs vs 11 +/- 14 msec, p less than 0.002). In conclusion PAF has an high incidence in the early follow-up of CABG operation and occurs independently of the type of caval cannulation. The presence of a major dispersion of intra right atrial conduction together with an high incidence of fractionizing potentials already before cardioplegia in the pts with AF suggests that the atria with intrinsic conduction delays can be per se predisposed to develop atrial tachyarrhythmias during the early follow-up.
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