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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 83 women younger than 46 years with acute myocardial infarction (MI) and 154 controls. There was a strong positive association between MI and the following: (1) age, (2) both oral contraceptive and noncontraceptive estrogen use, (3) cigarette smoking, and (4) the presence of predisposing medical conditions, eg, past MI, hypertension, and diabetes. ABO blood type and family history of arterial disease were also positively associated with MI. Whereas the risks for idiopathic stroke and venous thromboembolism have also been shown to be increased among oral contraceptive users, there is comparatively little correlation between these two illnesses and age or smoking in young women. The present study, taken together with previously published work, provides reasonable estimates of the vascular risks associated with oral contraceptive use.
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PMID:Myocardial infarction and other vascular diseases in young women. Role of estrogens and other factors. 71 57

Hemodynamic studies were carried out in 19 patients with left ventricular failure complicating acute myocardial infarction. Fourteen patients were studied before and after the intravenous administration of 0.5 mg/kg of furosemide, and five patients served as a control group. Serial measurements included intracardiac pressures, cardiac output and lung water by a double isotope technique. A significant reduction was noted in right atrial (P less than 0.005), pulmonary arterial (P less than 0.0005) and pulmonary wedge pressures (P less than 0.0005) after administration of furosemide. Only the change in right atrial pressure was significantly different from that in the control group (P less than 0.05). Lung water was not changed in 4 patients studied 2 hours after administration of furosemide but was significantly changed in the remaining 10 patients studied 4 to 24 hours after furosemide (P = 0.0001). This change was also significantly different from values in the control group (P less than 0.05). The patients with no reduction in excess lung water also had a smaller reduction in pulmonary wedge pressure and a lower pretreatment stroke work index than the other patients. The mobilization of excess lung water in patients with acute myocardial infarction complicated by left ventricular failure has several features. Despite a prompt diuresis, the reduction in lung water is delayed for at least several hours after the administration of furosemide and may be related to the degree of left ventricular dysfunction. Venodilation may be a major result of treatment with furosemide.
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PMID:Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction. 75 75

Correlation of left ventricular filling pressure (55 patients) with the left ventricular stroke work index (61 patients) provided a rapid means of objectively determining ventricular performance after myocardial infarction. Pressure was monitored by means of the Swan-Ganz balloon-tipped catheter and thermal indicators were used for measuring cardiac output. A hemodynamic grouping of these myocardial infarction patients on the basis of the stroke work index showed close correlation with morbidity and mortality and provided a more accurate prognostic indicator than did the commonly used clinical predictors. Serial assessment of ventricular function further aided in defining the prognosis when it was not clear on admission. Thus, the levels of normal or abnormal ventricular function and the effect of therapeutic measures can be rapidly evaluated by determining the pressures and flows in patients with acute myocardial infarction.
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PMID:Clinical implications of left ventricular function in patients with acute myocardial infarction. 78 53

Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.
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PMID:Intravenous nitroglycerin in acute myocardial infarction. 80 31

Fourteen patients with acute myocardial infarction were given 0.3 mg sublingual nitroglycerin within the first 12 hours of their acute myocardial infarction. Five minutes after sublingual nitroglycerin mean arterial pressure fell 9 mmHg (1.2 kPa) and remained significantly reduced for 30 minutes. Pulmonary capillary wedge pressure fell from a mean control value of 17 to 12 mmHg (2.3 to 1.6 kPa) and also remained reduced for 30 minutes. Heart rate was significantly raised and stroke work index reduced at five minutes. Patients with a stroke work index of greater than 55 g m per m-2 b.s.a. responed to nitroglycerin with a fall in both pulmonary capillary wedge pressue and strokework index while in those with a stroke work index of less than 55 g m per m-2 b.s.a. stroke work index did not fall concomitantly with the fall in pulmonary capillary wedge pressure. In one patient, nitroglycerin led to a precipitious fall in arterial pressure andrecurrence of chest pain.
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PMID:Role of sublingual nitroglycerin in patients with acute myocardial infarction. 80 10

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.
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PMID:Hemodynamic effects of nitroglycerin in acute myocardial infarction. 80 94

The hemodynamic effects of nitroglycerin ointment were studied in 22 patients with acute myocardial infarction. Control measurements were obtained and observations were made over the ensuing 240 minutes. There was no change in heart rate, cardiac index or stroke index. Ninety minutes after application of the ointment, peak decrements were evident in mean arterial pressure (from 100 to 88 mm Hg) (P less than 0.001), pulmonary capillary wedge pressure (from 19 to 13 mm Hg) (P less than 0.001), right atrial pressure (from 8 to 5 mm Hg) (P less than 0.001) and heart X systolic blood pressure (from 1,155 to 1,044 mm Hg/min X 10(-1) (P less than 0.02); significant changes were still present at 240 minutes. Total peripheral resistance decreased maximally from 19.8 to 17.2 units (P less than 0.02); the transmyocardial gradient (arterial diastolic -- pulmonary capillary wedge pressure) did not decrease during the study. These data indicate that nitroglycerin ointment improves cardiac performance in patients with acute myocardial infarction while reducing the determinants of myocardial oxygen consumption and preserving the transmyocardial gradient for coronary blood flow.
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PMID:Nitroglycerin ointment in acute myocardial infarction. 82 9

In 50 patients with proven acute myocardial infarction (AMI), left ventricular hemodynamics (pulmonary end-diastolic pressure [PAEDP]; cardiac index [CI]; stroke volume index [SVI]; and SVI/PAEDP were related to the size of the acute infarct. Acute infarct mass was calculated from serial determinations of serum creatine phosphokinase (CPK) every two hours, using a computer program. In 15 cases postmortem measurement of acute infarct size after staining with Nitro-BT was made and correlated with calculated infarct size. Correlation in this limited number of cases was good with a mean difference of 7 g. Acute infarct mass in 38 survivors was 46 +/- 5 g and was significantly smaller (P less than 0.05) than in the 12 nonsurvivors (76 +/- 12 g.) PAEDP in surviving patients was significantly lower (17 +/- 1 mm Hg) and SVI (36 ml/m2) and SVI/PAEDP (2.4 ml/m2/mm Hg) significantly higher than in the nonsurvivors (PAEDP: 24 mm Hg; SVI: 23 ml/m2; SVI/PAEDP: 0.86 ml/m2/mm Hg) (P less than 0.001 for all differences). Similar significant differences were observed between patients not in shock and those in cardiogenic shock. Although in 39 patients, in whom the infarction was their first, infarct mass was larger (58 +/- 6 g) than in 11 patients with repeat infarctions (37 +/- 8 g), left ventricular hemodynamics were slightly more impaired in reinfarctions (PAEDP: 21 +/- 3 mm Hg; CI:2.60 L/min/m2) than in first infarctions (PAEDP: 18 +/- 1 mm Hg; CI:2.82 L/min/m2). The occurrence of cardiogenic shock was a strong predictor of death; however, the wide scatter of the data for the parameters cardiac index, PAEDP, and acute acute infarct mass precluded their usefulness, when taken individually, in predicting survival. When a relationship between hemodynamics and infarct size was looked for, four constellations of individual patients were identified. These groups were defined by PAEDPs of above or below 18 mm Hg and infarct sizes above or below 65 g. Class A patients (N = 22) had a small infarct (29 +/- 4 g) and good pump function (PAEDP: 13 mm Hg; SVI: 40 ml/m2; SVI/PAEDP: 3.27 ml/m2/mm Hg); prognosis was good for these patients. In class B (N = 13) the infarct was large (96 +/- 8 g) and pump function markedly impaired (PAEDP: 26 mm Hg; SVI: 24 ml/m2; SVI/PAEDP: 0.98 ml/m2/mm Hg); 54% of these patients died. Five patients in class C had, in the presence of a large infarct (84 g), only a slightly elevated PAEDP of 17 mm Hg and an almost normal SVI of 37 ml/m2. In contrast, the ten class D patients had an infarct size (34 g) similar to that in class A, but high PAEDP (23 mm Hg) and moderately reduced SVI (31 ml/m2). In this group a high incidence of reinfarctions (six out of ten) occurred. It is concluded that infarct mass calculated from serial CPK analysis, as a single parameter, cannot be used to predict mortality or development of cardiogenic shock in an individual patient.
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PMID:Infarct size estimated from serial serum creatine phosphokinase in relation to left ventricular hemodynamics. 83 46

Enhanced electrical stability of acutely ischemic myocardium with vagal stimulation and acetylcholinesterase inhibition has been demonstrated experimentally. To extend these findings clinically, within 24 hours of acute myocardial infarction, 11 patients underwent continuous 10 hour Holter monitoring: 2.5 hour control before and after 5 hour constant edrophonium infusion (0.25 to 2.00 mg./minute). Continuous infusion of the agent lowered heart rate 92 to 78 b.p.m. (p less than 0.01). Although mean total ventricular extrasystoles (PVC's) per 5 hours per patient (131) and PVC's per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVC's: multifocal, R on T, paried, greater than 5 per minute or ventricular tachycardia) were terminated in six of 10 patients by edrophonium. However, serious ventricular arrhythmias continued in three patients and appeared in four despite the agent. Ventricular fibrillation did not occur during the 10 hour period of study. In addition, the patients were evaluated hemodynamically and by His bundle electrograms before and after a 10 mg. bolus of edrophonium prior to the 10 hour constant infusion: heart rate declined (88 to 72 b.p.m., p less than 0.01), while mean arterial pressure (98 mm. Hg), left ventricular filling pressure (14 mm. Hg), cardiac index (2.4 L. per minute per square meter), and stroke work index (36 Gm.m./M.2) were unchanged (p greater than 0.05). The edrophonium bolus prolonged the A-H interval (117 to 135 msec., p less than 0.01) while the H-Q interval was unaltered (48 msec; p greater than 0.05). It is concluded that increased vagal tone with edrophonium did not reduce the over-all presence of premature ventricular contractions in the entire study group; however, the malignant nature of PVCs and ventricular tachycardia appeared to be lessened by the parasympathomimetic agent in certain patients. In addition, no adverse hemodynamic or intraventricular conduction effects were produced by edrophonium administration.
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PMID:Clinical evaluation of the enhancement of vagal tone in acute myocardial infarction by edrophonium hydrochloride: effects on ventricular arrhythmias, His bundle electrography, and left ventricular function. 83 66

In a three-year prospective study of acute cerebrovascular accident patients admitted to a geriatric unit within 72 hours of the onset, 12.7% had what was considered to be an associated acute myocardial infarction. In the majority of cases, 71%, there was no clinical indication of an acute myocardial infarction and, had it not been for electrocardiographic and enzyme studies, the concurrence of these two conditions might not have come to light. The possible explanations for the concurrence of these two conditions are explored. Patients were followed-up for five years. The mortality rate for the combined acute myocardial and cerebral infarction cases admitted to hospital was 53% in six weeks, and 64% in one year, compared with 26% and 42%, respectively, in those strokes uncomplicated by a cardiac infarction. Only one patient has survived for five years. The recognition of such cases is important in terms of management and prognosis and this may be achieved by ECG recordings followed by enzyme studies in all cases of acute stroke admitted to hospital.
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PMID:Myocardial infarction coincident with cerebrovascular accidents in the elderly. 84 3


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