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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of prostaglandins (PGs) in cardiac pathophysiology has been reviewed with special emphasis on clinically applied aspects. Several PGs are synthesized and released by the heart and coronary vessels. Their synthesis is altered by various factors such as physical manipulation of tissue, pharmacological treatments and pathological conditions such as myocardial over-reactivity and ischemia. The involvement of PGs in cardiac dysfunction remains controversial, although it has been proposed that various PGs such as PGI2 or PGB2 may play a role in disaggregating platelets, inhibiting thrombus progression and coronary vasodilatation. The balance between thromboxane A2 (TXA2), a proaggregatory agent released from platelets and PGI2 may have a role in the genesis and management of angina and myocardial infarction. The use of non-steroidal anti-inflammatory agents in these conditions remains controversial; their possible beneficial effects are believed to be due to inhibition of TXA2 synthesis whereas their failure to be effective may be a consequence of concomitant inhibition of PGI2 production. Modulation of endogenous PG synthesis and administration of exogenous PGs or their analogues appear to be two therapeutic approaches in the management of certain cardiac diseases. Accordingly, there is a great need for synthesizing stable and potent PG analogues as well as specific inhibitors of PG synthesis in addition to studying their pharmacology and therapeutics. In this review we have emphasized the involvement of PGs in the pathogenesis of some forms of cardiac disease and have highlighted some therapeutic implications of these substances for the treatment of heart disease.
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PMID:Prostaglandins and heart disease. 385 Jul 65

The recent deaths of two workers with coronary artery disease (CAD) following exposure to carbon monoxide (CO) at work reinforced our appreciation of the hazard of this exposure to individuals with preexisting heart disease. Carbon monoxide acts to precipitate ischemia by reducing oxygen delivery to the myocardium. Animal and in vitro experiments suggest that CO may accelerate the development of atherosclerosis, particularly if exposure is in association with other risk factors. Thus, persons with known CAD who are exposed to CO at work are at risk for both the acceleration of the course of the underlying disease and for precipitation of acute ischemia or infarction following excessive exposure. Particular attention should be given to control of CO exposures in light of this hazard. For various reasons, preplacement evaluations or other job selection procedures do not adequately address his hazard. In view of the high prevalence of CAD in the U.S. and the high frequency of workplace exposure to CO, particular attention should be given to control of CO exposure through industrial hygiene measures.
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PMID:Exacerbation of coronary artery disease by occupational carbon monoxide exposure: a report to two fatalities and a review of the literature. 388 38

The arterial-coronary sinus lactate difference was measured in 17 patients after each step of a programmed ventricular stimulation protocol consisting of single, double, and triple extrastimuli, first at a basic drive cycle length of 600 msec, then at 400 msec, with an inter-train interval of 4 seconds. Four patients had no structural heart disease, four had an idiopathic dilated cardiomyopathy, and nine had coronary artery disease with a significant stenosis in at least one branch of the left coronary artery. Net myocardial lactate production during programmed ventricular stimulation was observed in three patients with coronary artery disease, but not in any patient without coronary artery disease. Among the patients who had coronary artery disease, net myocardial lactate production generally occurred in the patients who had more severe coronary artery disease. Exercise-induced ischemia, as demonstrated by a stress thallium-201 test, did not correlate with myocardial lactate production during programmed ventricular stimulation. Programmed ventricular stimulation, with a stimulation protocol typically used in many electrophysiology laboratories, is capable of inducing myocardial ischemia in at least some patients who have coronary artery disease. This finding suggests that myocardial ischemia may potentially influence the results of programmed ventricular stimulation in some patients with coronary artery disease.
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PMID:Effect of programmed ventricular stimulation on myocardial lactate extraction in patients with and without coronary artery disease. 394 67

Two young males who had no organic heart disease died unexpectedly during the night. In one patient, the monitor ECG showed a sinoatrial block and the electrophysiologic study revealed a sinoatrial conduction time at the upper limit of normal and a prolonged PA interval. The surface ECG showed left axis deviation. Ventricular ectopic beats were confined to the night when he died from ventricular flutter. The ECG of the other patient was normal except for the change in QRS configuration found when the preceding RR interval was prolonged, suggesting a phase 4 block in intraventricular conduction. He was completely free from arrhythmia except for the ventricular ectopic beats which developed around 9:00 p.m. and the ventricular flutter following an R-on-T type ventricular ectopic beat which resulted in death during the night. The autopsy showed no organic heart disease. ST elevation suggestive of acute ischemia was not found and the QT intervals were normal in both cases. No electrolyte imbalances were found. These 2 cases can be diagnosed as pokkuri disease which is well known in Japan. The victims are exclusively young males who have no apparent diseases to which death can be attributed.
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PMID:Sudden nocturnal death in young males from ventricular flutter. 405 56

The apexcardiogram (acg), when recorded serially in patients with acute myocardial infarction (ami), preinfarction angina (pia) and stable ischemic heart disease (ihd), appeared to reflect the abnormal patterns of contraction of the left ventricle in these conditions. Thus, paradoxical bulging (dyskinesis) of the systolic wave or increased "a" wave amplitude with gradual recovery over several weeks was found in all 60 patients with documented ami and in 18 of 20 patients with pia. Electrocardiogram changes were noted, however, in only eight of the pia patients. Changes in the acg frequently antedated ischemia in the ecg. Paradoxical bulging of the systolic wave of the acg was additionally noted in patients during the pain of angina pectoris but this promptly disappeared after the administration of nitroglycerine. Patients with classic angina often had normal resting ecg's but abnormal resting acg's. In contrast to the relatively transient abnormalities noted above, the acg remained unchanged in most patients with stable ihd during follow-up of three months to two years. Patients undergoing coronary bypass operations, however, showed immediate improvement in the acg in the postoperative period. These results suggest the acg reflects the contractile pattern of the left ventricle, and may be an indirectly recorded ventriculogram. Its enhanced sensitivity and the earlier development of changes in comparison to the ecg make this a valuable tool in the study of patients with heart disease.
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PMID:The apexcardiogram in ischemic heart disease. 500 98

A beta-adrenoceptor antagonist, bisoprolol, was given by mouth, 5 and 10 mg doses per 24 hours, in a double-blind randomized cross-over trial to 12 patients with stable coronary-heart disease. Ischaemia criteria proved not reproducible in control ergometry tests on two patients, leaving ten patients for further evaluation. On two days, one week apart, bicycle ergometry was undertaken until the occurrence of ST segment depression of at least 0.3 mV, often associated with angina. Four, eight and 24 hours after the drug had been taken, the ergometry was repeated to the same maximal Watt level and duration of exercise. Heart rate and pressure-rate product at rest, as well as the same parameters including ST segment depressions immediately at the end of exercise, significantly fell after bisoprolol during the entire trial period independently of the dose. There was no sign of reduced effectiveness 24 hours after drug intake. The results indicate that treatment of stable angina with bisoprolol can be achieved with a single daily dose.
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PMID:[Effect of bisoprolol in coronary heart disease. Effect on cardiovascular parameters and ischemic ST depression: studies on the duration of the effect]. 615 Aug 39

Mortality and amputations after limb ischemia following thromboembolic obstruction show no significant improvements despite the technical progressions based on the use of Fogarty catheter. The Author analizes 98 patients surgically treated, to point out the reasons of failures: 14,5% mortality and 11% amputations in embolic ischemia and 11% and respectively 16% in acute thrombosis; the age resulted over 70 in 70% of patients; in the 75% embolic origin was determined by a atherosclerotic senile cardiopathy. In case of embolic ischemia, highly significantly from a statistical point of view worse results were observed for proximal obstructions. In overall patients must be noted a mortality of 6% under the age of 60 and 22% over this age. Finally, once again considering the embolic obstruction, the length of ischemic time was observed directly correlated with functional results.
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PMID:[Acute ischemia of the extremities caused by thromboembolism]. 621 3

One hundred and eighty-one patients (101 men and 80 women) underwent 61 congenital and 120 acquired heart operations using cold blood potassium cardioplegia as the method of myocardial protection at Kagoshima University from August, 1978 to August, 1981. Hospital deaths occurred in 18 patients (9.8%), and 4 cases were late death (2.2%). Multivariate analysis revealed no significant relationship between type of heart disease and operative mortality or the occurrence of post-operative low output syndrome. To evaluate the superiority of cold blood cardioplegia for myocardial protection, we carried out 20 orthotopic heart transplants in dog; 16 transplanted grafts could maintain the circulation of recipient without cardiopulmonary bypass. Cardiac contractility following 90-minute ischemic time showed 97 to 100% of the control values without any inotropic drugs. These clinical and experimental findings suggest that cold blood potassium cardioplegia provides excellent myocardial protection during the ischemia of the heart.
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PMID:[Myocardial protection with cold blood potassium cardioplegia: experimental and clinical studies]. 637 82

A 62-year-old man who was under observation following an episode of severe chest pain developed complete heart block and hypotension after receiving sublingual nitroglycerin. The reaction occurred while the patient was receiving an intravenous maintenance infusion of lidocaine but did not occur in response to either nitroglycerin alone or lidocaine alone. There was no evidence of acute cardiac ischemia nor of clinically significant underlying heart disease. Complete heart block after sublingual nitroglycerin in the absence of significant cardiac disease is an exceedingly rare phenomenon.
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PMID:Complete heart block after sublingual nitroglycerin. 640 6

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of ventricular tachycardia. 646 97


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