Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment strategies for daily life silent myocardial ischemia: a correlation with potential pathogenic mechanisms. 135 7

The electrophysiologic and antiarrhythmic effects of ibutilide, sotalol, and encainide were compared in dogs 24 h after myocardial infarction. Ibutilide (0.03 to 0.3 mg/kg i.v.) prevented the induction of ventricular arrhythmias in 100% of the dogs that had demonstrated inducible ventricular arrhythmias prior to treatment. This antiarrhythmic action was associated with significant increases in ventricular refractoriness and monophasic action potential duration. Sotalol (1.0 to 10.0 mg/kg i.v.) increased the ventricular refractory period and monophasic action potential duration and prevented the induction of ventricular arrhythmias in 75% of the dogs that demonstrated inducible ventricular tachyarrhythmias at baseline. Although 10 mg/kg of sotalol was required to prevent the initiation of ventricular tachycardia, this dose produced marked cardiovascular depression and hypotension in 50% of the dogs tested. Neither ibutilide nor sotalol significantly decreased the incidence of spontaneous ventricular arrhythmias. The class IC agent encainide (0.3 to 3.0 mg/kg i.v.) was successful in preventing the induction of ventricular arrhythmias in only 20% of the dogs tested. However, in contrast to ibutilide and sotalol, encainide significantly reduced spontaneous arrhythmias. Atrial and ventricular refractoriness were significantly increased only after the highest dose of encainide tested (3.0 mg/kg). Over the dose ranges studied, the relative efficacy for prevention of pacing-induced ventricular arrhythmias was ibutilide greater than sotalol much greater than encainide. For suppression of spontaneous ventricular arrhythmias, the relative efficacy was encainide much greater than ibutilide = sotalol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ibutilide on spontaneous and induced ventricular arrhythmias in 24-hour canine myocardial infarction: a comparative study with sotalol and encainide. 137 95

Effects of SUN-1165, a class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the effective refractory period (ERP) were examined in a canine model of myocardial infarction and compared with those of lidocaine. The antiarrhythmic effects were examined on the arrhythmias developed 24 h after left anterior descending coronary artery (LAD) ligation and ventricular premature stimulation-induced arrhythmias 5-7 days after LAD ligation. Effects on intraventricular conduction and ERP were also examined in animals 5-7 days after LAD ligation. The intraventricular conduction time (CT) was determined by excitation induced by a ventricular stimulation at various coupling intervals from 200 to 1,000 ms. SUN-1165 (1 and 3 mg/kg) showed a marked reduction in the frequency of ventricular ectopic beats 24 h after LAD ligation and was more potent than lidocaine. SUN-1165 (1 and 3 mg/kg) prolonged CT in the infarcted zones over a wide range of the coupling intervals and produced block of severely delayed conduction. In contrast, lidocaine prolonged CT only at short coupling intervals. Ventricular premature stimulation produced ventricular arrhythmias, which were prevented by pretreatment with SUN-1165 (3 mg/kg). ERP was prolonged by SUN-1165 (3 mg/kg). In conclusion, SUN-1165 showed antiarrhythmic effects in a canine model of myocardial infarction. A selective depression of delayed conduction in the infarcted zone and a prolongation of ERP probably contribute to this antiarrhythmic effect.
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PMID:Effects of SUN-1165, N-(2,6-dimethylphenyl)-8-pyrrolizidine acetamide hydrochloride hemihydrate, a new class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the refractory period in canine myocardial infarction. 137 23

Twenty-four hour Holter monitoring and symptom-limited exercise testing were carried out prior to discharge in 157 patients recovering from acute myocardial infarction. Supraventricular arrhythmias (SVT) during Holter monitoring were recorded in 15%, and ST segment depression during exercise in 27%. No association between exercise-provoked ischaemia and SVT was found in the late hospital phase of myocardial infarction. After the tests, patients were double-blindly randomized to treatment with verapamil 120 mg t.i.d. or placebo. One month after randomization 24 h Holter monitoring was repeated in 125 patients (verapamil = 63, placebo = 62). At one month a significantly increased incidence of SVT was found in the placebo group (25%) compared to the verapamil-treated patients (9%) (P = 0.04). The increased prevalence in the placebo group was mainly due to an increased incidence of SVT in patients with exercise-induced ischaemia (P = 0.03). This increment was blurred in the verapamil group. In conclusion, the prevalence of SVT increases during the first month after myocardial infarction. The increase is most pronounced in patients with residual myocardial ischaemia and seemed to be prevented by treatment with verapamil.
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PMID:The significance of myocardial ischaemia and verapamil treatment on the prevalence of supraventricular tachyarrhythmias in patients recovering from acute myocardial infarction. Danish Study Group on Verapamil in Myocardial Infarction. 139 20

In this case report a 30-year-old woman suffering from progressive angina pectoris and dyspnea, having been operated on previously for atrial septum defect at the age of 19 and later aged 24 for coarctation of the aorta, is described. Upon observation, patient showed cardiac symptoms already under mild stress and remained resistant to nitroglycerin. Rest-ECG and serum cardiac enzymes were repeatedly without findings, while stress-ECG at a level of 100 W showed a ST-segment depression of 0.15 mV, at the same time complaining of angina pectoris symptoms. Coronary angiography revealed a left circumflex coronary artery arising from the left atrium being fully supplied by the left anterior descendent artery and the right coronary artery via pronounced collaterals, both originating from the ascending aorta. Despite such severe symptoms patient refused surgery suturing the abnormally arising artery. One year following coronary angiography patient is suffering from stabile angina pectoris without occurrence of myocardial infarction or another cardiovascular event.
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PMID:[Abnormal origin of the ramus circumflexus sinister from the left atrium in a 30-year-old patient with aortic isthmus stenosis and atrial septal defect]. 141 69

To determine the effects of myocardial infarction-induced left ventricular failure on the mechanical characteristics of the remaining viable myocytes, coronary arterial occlusion was performed in rats, and cell function was examined 1 wk later. Moreover, to establish the mechanisms by which treatment with angiotensin-converting enzyme inhibitors ameliorates cardiac dynamics, captopril was administered immediately after surgery, and the contractile behavior of the unaffected cells was similarly analyzed 7 days later. The severe impairment in left-side pump function was found to be associated with a decrease in the velocities of myocyte shortening and relengthening and peak shortening despite a prolongation of contraction duration. In addition, a uniform property was recognized in myocytes from infarcted and noninfarcted hearts. Longer cells manifested greater velocity of shortening, whereas wider cells of identical length exhibited depressed shortening velocity. After infarction, the depression in cell contractility coupled with lateral expansion of myocytes exceeded the influence on cell mechanical behavior linked to myocyte lengthening leading to an overall decrease in contractility of the hypertrophied cells. Captopril therapy preserved, in part, the ability of myocytes to shorten and relengthen, which was accompanied by a decrease in the lateral and longitudinal expansions of these cells.
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PMID:Mechanical performance of spared myocytes after myocardial infarction in rats: effects of captopril treatment. 141 11

Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The annual incidence was 22 cases per million population. Twenty-two cases had pre-existing cardiac disease, mainly valvular disease-usually rheumatic (nine cases) and prosthetic valves (10 cases). Recognizable precipitants such as recent surgery were uncommon. Two cases presented after deliberate drug overdose possibly due to depression exacerbated by systemic disease. Symptoms were usually non-specific. All but two cases had murmurs and most were pyrexial. Splinter haemorrhages and clubbing were seen in about 20% of cases. Viridans-type streptococci were the commonest infecting organisms (14 cases). Staphylococcal infection (six cases) was confined to intravenous drug abusers and patients with prosthetic valves. Five cases were culture negative. Cardiac failure was present in 13 cases at presentation and developed in seven others during treatment. Acute valve replacement was necessary in eight cases, and late replacement in three. Renal impairment (plasma urea > 8 mmol/l and/or plasma creatinine > 120 mumol/l) occurred in 19 cases during the course of their illness. Embolic phenomena occurred in 12 patients and mostly involved the central nervous system. In the 8 fatal cases, the cause of death was cardiac failure in six, cerebrovascular accident in one, and myocardial infarction in one. Four of the six patients who subsequently died of cardiac failure had been referred for surgery. Both those who were not referred had coexisting medical problems. Factors associated with increased mortality were age, male sex, cardiac failure (P < 0.01), renal impairment (P < 0.05), and embolic phenomena (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infective endocarditis in a district general hospital. 143 86

We studied the clinical significance of electrocardiographic ST segment changes during PIA attacks. Of 478 AMI patients admitted to the CCU of our hospital within 48 hours after onset, we evaluated 73 (15.3%) with PIA. According to electrocardiographic ST segment changes during PIA attacks, the patients were divided into three groups, namely ST elevation at the same infarction site (same site elevation group), ST depression at the same site (same site depression group), and ST depression at other sites (other site depression group), and their pathological condition was studied. There were 33 patients (45.2%) in the same site elevation group, 19 (26.0%) in the same site depression group, and 21 (28.8%) in the other site depression group. The predominant infarction areas were anteroseptal and inferior wall in the same site elevation group, NTMI in the same site depression group, and inferior wall in the other site depression group. PIA usually occurred within 4 days after the onset of infarction in the same site elevation group, and within 5-7 days in the other site depression group, but no uniform trend was observed in the same site depression group. With respect to the number of vessels showing disease, cases of single-vessel disease tended to predominate in the same site elevation group, while cases of three-vessel disease tended to predominate in the same site depression group and the other site depression group. Stenosis rates in the vessels responsible for infarction were high in the same site elevation group in the acute period. Prognoses were poorest in the same site depression group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinical study of postinfarction angina (PIA): the significance of electrocardiographic ST segment changes during anginal attacks]. 143 76

To determine the effects of exercise training on exercise-induced ischemia in patients following myocardial infarction, the experience of 13 patients with exercise-induced ST depression, who were moderate-to-high intensity trained for 1 year, has evaluated. After training, the maximum ST depression was significantly less (1.9 +/- 0.8 vs. 1.1 +/- 0.8 mm; p < 0.01), despite an increased maximal rate-pressure product (RPP; heart rate x blood pressure/100; 241.3 +/- 44 vs. 262.0 +/- 58; p < 0.01). For the onset of 0.1 mV of ST depression, we found a significant increase in RPP from 204.1 +/- 34.7 to 234.1 +/- 49.4 (p < 0.01) and also in heart rate (117.1 +/- 15.1 vs. 125.1 +/- 21.7 b.p.m.; p < 0.05), blood pressure (167.6 +/- 18 vs. 180.3 +/- 18 mm Hg; p < 0.01) and workload (93.8 +/- 17.4 vs. 121.1 +/- 23.2 W; p < 0.01). The relationship between ST depression and RPP (RPP/STmax) was favorably modified after training. The ratio RPP/STmax improved significantly from 143.6 +/- 49.4 to 209.1 +/- 69.5 (p < 0.0001). These findings support the hypothesis that a 1-year moderate-to-high training program in some patients following myocardial infarction can elicit adaptations that may well be attributed, at least in part, to an improvement in coronary blood flow.
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PMID:Effects of a 1-year exercise training program on myocardial ischemia in patients after myocardial infarction. 145 Nov 28

We studied 141 patients to evaluate the pathogenesis and clinical picture of high-risk unstable angina (UA), designated as impending myocardial infarction (IMI) in this study, or severe early post-infarction angina (PIA). IMI and PIA were diagnosed when chest pain appeared at rest and lasted 15 min or more despite extensive pharmacological therapy during hospital stay among consecutive 510 patients with UA. All patients underwent coronary angiography urgently within 72 h after chest pain, and were divided into 2 subgroups according to ST segment shifts during chest pain. In IMI, 42 patients with ST depression had higher incidences of prior myocardial infarction (MI), worsening UA, multivessel disease and complex lesions such as eccentric irregular lesion or ulceration. On the contrary, in 44 with ST elevation, new onset UA, single vessel disease and coronary thrombus (CT) were dominant. In PIA, 32 patients with ST elevation revealed higher incidences in Q wave MI, ST elevation at the MI onset, single vessel disease and CT, compared to 23 with ST depression who showed a high proportion of complex lesions. Thus, it was evident that there was a common link between the pathogenesis of IMI and PIA. The therapeutic options were also different in the groups according to ST segment shift. We conclude that ST segment shifts during chest pain may be useful for determining the pathogenesis and clinical features of high-risk UA.
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PMID:Pathogenesis, treatment and prognosis of impending myocardial infarction and early post-infarction angina--relation between ST-segment shift during myocardial ischemia and the pathogenesis. 145 39


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