[Electrocardiographic study of ventricular inversion with transposition of the great vessels. Apropos of 26 cases].
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Biomedical subjects
Publications and source records attributed to J J Poveda.
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OBJECTIVES: To assess changes in heart rate and cardiac arrhythmias during anaesthetic induction and tracheal intubation in patients undergoing cardiac surgery. MATERIAL AND METHODS: 79 patients scheduled for cardiac surgery were divided into three groups: group I, 36 valvular diseases with a good ventricular function, group II, 22 valvular diseases with an ejection fraction less than 0.5, and group III, included 21 patients with coronary artery disease. All patients had a Holter monitoring. Anesthesia was performed with diazepam and morphine in patients with valvular disease and with diazepam and fentanyl in those with coronary artery disease. RESULTS: During anesthesia induction there were no significant increases in heart rate in the two groups of patients with valvular diseases: in group I (n = 36, with good ventricular function) heart rate increased by about 5.4 +/- 23% and in group II (n = 22, with ejection fraction less than 0.5) by 7.5 +/- 33%. In patients with coronary artery disease (n = 21) we did not observe significant decreases in heart rate (-4.28 +/- 17%). During tracheal intubation the heart rate increased by 15.9 +/- 30% in group I (p < 0.002), by 13.6 +/- 30% in group II (p < 0.02), but decreased by 1.19 +/- 23% (p = NS) in patients with coronary artery disease. During anesthetic induction we observed frequent premature beats (single forms) in 13.8% of patients in group I, 13.6% in group II, and 9.5% in group III. The incidence of this arrhythmia during tracheal intubation was 16.6%, 9%, and 14%, respectively for the three groups. Sustained ventricular tachycardia was only observed in one patient. CONCLUSIONS: Changes in heart rate and ventricular arrhythmias occurring during anesthetic induction and tracheal intubation in patients undergoing valvular and coronary surgery were infrequent and not severe.
Nitroglycerin (glyceryl trinitrate) is a substance that is metabolized to nitric oxide in the cell. Its action is not dependent of the endothelium derived nitric oxide, but imitates those of this biological mediator. We thought that nitroglycerin should have the same in vivo actions as the endogenous nitric oxide in vitro has. We report and discuss the first patient with superficial thrombophlebitis successfully treated with transdermal nitroglycerin.
The long-term prognosis after heart transplant is mainly determined by the development of transplant vasculopathy. The pathogenic mechanism of transplant vasculopathy remain uncertain, although endothelial dysfunction has been postulated. The objective of this work is to evaluate the smooth muscle and endothelium nitric oxide relaxing mechanisms in coronary arteries from patients with transplant vasculopathy. We studied human coronary arteries obtained from heart transplant surgery specimens of patients with heart transplant vasculopathy, ischaemic cardiopathy or dilated cardiomyopathy. Rings from the coronary arteries were mounted on stainless steel hooks in 40 ml organ bath. The tissues were contracted with phenylephrine (approx. ED 80-90) and concentration-response curves were performed with glyceryltrinitrate and acetylcholine. Glyceryltrinitrate relaxed arterial rings from patients with dilated cardiomyopathy and ischaemic cardiopathy. Arterial rings from patients with heart transplant vasculopathy showed a lower response to glyceryltrinitrate. Acetylcholine induced dilatation of coronary arteries from dilated cardiomyopathy but increased the tension in coronary rings from heart transplant vasculopathy and inschaemic cardiopathy. In conclusion, there is a lower response to glyceryltrinitrate and a paradoxical response to acetylcholine in arteries from patients with transplant vasculopathy. The response to glyceryltrinitrate may be a meaningful tool in the early diagnosis of transplant vasculopathy.