Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the efficacy and safety of the ultra short-acting beta-blocking agent, esmolol, in acute unstable angina, we administered esmolol to 21 patients who had persistent angina despite conventional medical therapy. Following a baseline Doppler echocardiographic examination, esmolol was titrated to reduce the rate-pressure product by at least 20%. Once the patients had been receiving a maintenance dosage for 30 minutes, Doppler echocardiographic studies were repeated. Mean esmolol dose at target response was 17 +/- 16 mg/min, with the dosage range of 8 to 24 mg/min. Esmolol was effective in alleviating anginal chest pain in 18 of the 21 patients. Seven patients eventually underwent percutaneous transluminal coronary angioplasty (PTCA) and eight had coronary bypass surgery. The remainder were discharged receiving medical therapy including oral beta-blockade. During esmolol therapy, heart rate and blood pressure decreased significantly (86 +/- 14 to 68 +/- 12 beats/min and 125 +/- 16 to 103 +/- 20 mm Hg, both p less than 0.001). Cardiac output decreased from 5.4 +/- 1.3 to 4.5 +/- 1.1 L/min (p less than 0.001) secondary to a decrease in heart rate as stroke volume remained unchanged. Left ventricular ejection fraction increased from 47 +/- 12 to 49 +/- 13 with esmolol therapy, although this change was not statistically significant. Both the one third filling fraction as well as E/A ratio (ratio of early-to-late diastolic filling velocities) increased with esmolol therapy (35 +/- 8% to 38 +/- 8% and 0.73 +/- 0.2 to 0.85 +/- 0.23, both p less than 0.005), indicating improvement in left ventricular diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ultra short-acting intravenous beta-adrenergic blockade as add-on therapy in acute unstable angina. 167 51

Multiple clinical trials have demonstrated that thrombolytic treatment early in the course of acute myocardial infarction significantly reduces mortality. Patients under 75 years of age who have had chest pain for no longer than six hours and who demonstrate ST-segment elevation on electrocardiogram are the best candidates for this therapy. Recent studies suggest that there is little difference in effectiveness among streptokinase, alteplase and anistreplase. However, streptokinase is 10 times less expensive than the other agents and causes fewer intracranial bleeds, the major serious adverse effect of thrombolytic therapy. An advantage of anistreplase is that it can be given in a five-minute bolus injection, compared with a one-hour infusion for streptokinase and a three-hour infusion for alteplase. Thrombolytic therapy is contraindicated in patients with known pregnancy, active internal bleeding, uncontrolled hypertension, aortic dissection, intracranial neoplasm or a history of hemorrhagic stroke. Heparin should be administered with both alteplase and streptokinase. Aspirin, beta blockers, nitrates and lidocaine are useful adjunctive therapies in the setting of an acute myocardial infarction.
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PMID:Thrombolytic therapy in acute myocardial infarction. 173 49

The influence of elastic recoil and restoring forces on diastolic left ventricular pressure decay and minimum left ventricular pressures has been demonstrated in animal models but has not been studied in the human heart. To investigate this issue in the normal human left ventricle, we studied eight patients with chest pain and normal coronary arteries with simultaneous measurement of left ventricular volume (by radionuclide angiography) and pressure (by micromanometer catheter) and coronary sinus blood flow. Electrocardiographic-gated data were obtained in the basal state, during rapid atrial pacing, and during isoproterenol infusion to a similar heart rate. Compared with pacing, isoproterenol increased ejection fraction and reduced end-systolic volume (p less than 0.005), end-systolic pressure (p less than 0.005), and the half-time of pressure decline after peak negative dP/dt (T1/2) (p less than 0.001). Negative diastolic pressure developed in seven of eight patients during isoproterenol (range, -0.5 to -2.4 mm Hg) but in only one of eight during pacing (-0.2 mm Hg). These reduced diastolic pressures during isoproterenol were accompanied by increased stroke volume (reflecting increased transmitral flow) and diminished pulmonary wedge pressure (reflecting left atrial pressure). The magnitude of reduction in minimum diastolic pressure during pacing and isoproterenol was related to the change in end-systolic volume (r = 0.79, p less than 0.001), ejection fraction (r = -0.74, p less than 0.001), T1/2 (r = -0.57, p less than 0.02), and coronary sinus flow (r = 0.73, p less than 0.005). Stronger correlations were observed in analyzing changes during isoproterenol alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimum left ventricular pressure during beta-adrenergic stimulation in human subjects. Evidence for elastic recoil and diastolic "suction" in the normal heart. 197 48

In this study, we tried to characterize the changes in left ventricular (LV) function and coronary hemodynamics in patients with compensated hypertension (HT) who were free from coronary artery disease. The study group consisted of 10 men with compensated essential HT at ages 48-65 years (mean = 58). The durations of HT history for the various patients ranged from 5 to 14 years. Mean arterial pressure (MAP) was 122 +/- 2 mmHg at the time of study. The control group was composed of 8 men with mild mitral valve prolapse. They were studied because of chest pain with no demonstratable pathological conditions. Their ages ranged from 39 to 65 years (mean = 57). The MAP for controls was 86 +/- 3 mmHg. All patients in both groups underwent routine cardiac catheterization, coronary arteriography, and measurements of the coronary sinus (CS) and great cardiac vein (GCV) blood flows. Left ventricular muscle mass (LVMM), coronary resistance and coronary reserve were also derived from the hemodynamic study. There was a significant difference in the LVMM index between the study patients (114.9 g/m2) and the control subjects (96.8 g/m2, p less than 0.001). The LV function of the patients in the study group was essentially normal, but the following parameters were significantly different from those of the control subjects: cardiac index, stroke volume index, and dp/dtmax. There was a good correlation between repeated measurements of both the CS and GCV blood flows (r = 0.97 for both).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The coronary hemodynamics and left ventricular function in patients with compensated hypertension. 197 57

Systolic time intervals were obtained from 19 middle-aged noninsulin-dependent diabetic patients without clinically evident cardiovascular disease (8 patients had and 11 did not have retinopathy) and 14 normal subjects using ear densitography. All subjects had neither ischemic electrocardiographic response nor chest pain during maximal treadmill exercise. Although left ventricular ejection time (LVET) and preejection period (PEP) did not differ significantly at rest between the three groups, a prolongation of LVET with a nearly identical PEP response was observed during exercise in diabetic patients with retinopathy. These data indicate that the diabetic patients with retinopathy relied on the enhanced ventricular filling in maintaining stroke volume during exercise. Thus, retinopathy is associated with impaired left ventricular systolic function in noninsulin-dependent diabetic patients.
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PMID:Left ventricular dysfunction during dynamic exercise in noninsulin-dependent diabetic patients with retinopathy. 202 62

A clinicopathological analysis of myocardial infarction with an onset of stroke-like symptoms was carried out on 30 autopsy cases at the Tokyo Metropolitan Geriatric Hospital. The cases were classified into four groups according to the types of brain lesions, I: embolism (n = 17), II: thrombosis (n = 9), III: bleeding (n = 2), and IV: no remarkable focal lesion (n = 2). Classification was made based on clinical findings, and pathological features. The characteristic clinical findings were conciousness disturbance, no elevation of blood pressure at the onset of stroke, hemiplegia and shock. However, the typical anginal chest pain was found in only 17% of cases. The underlying diseases and complications were hypertension, atrial fibrillation (Af), disseminated intravascular coagulation (DIC), renal failure, malignant neoplasma, and diabetes mellitus. The incidences of Af, DIC, mural thrombus, non-bacterial thrombotic endocarditis (NBTE) were significantly higher in the group with cerebral embolism than in the group with cerebral thrombosis. The coronary stenotic index was also smaller in the group with cerebral embolism. Therefore, the major etiology of cardio-cerebral apoplexy was a simultaneous embolism to the brain and heart due to Af, NBTE or, DIC.
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PMID:[Myocardial infarction beginning with cerebral symptoms in 30 cases of cardio-cerebral apoplexy]. 204 62

All thrombolytic agents convert plasminogen to plasmin, either directly, as in the case of urokinase, saruplase, and alteplase, or indirectly, as in the case of streptokinase. In the majority of recent clinical trials with streptokinase, a high-dose (0.7-1.5 million units), brief-duration (30-90 minutes) drug regimen has been used. After a mean interval of 4.2 hours from onset of chest pain to intravenous infusion of streptokinase, repeat angiography performed 60-90 minutes after the start of thrombolytic treatment gave a reperfusion rate of 43%; the corresponding figures for anistreplase, saruplase, and alteplase are 56%, 67%, and 69%. The patency rates obtained in similar studies with the same end point are 56% for streptokinase, 77% for anistreplase, 62% for urokinase, 71% for saruplase, and 75% for alteplase. The in-hospital mortality in randomized trials (six large studies in a total of 31,713 randomized patients) with intravenous high-dose streptokinase decreased from 12.0% in the control group to 9.47% in the streptokinase group. In a mortality study involving 1,258 patients randomized to intravenous anistreplase or placebo, the 30-day mortality was reduced by 47%, from 12.2% to 6.4%. In a large trial in which 5,011 patients were randomized to alteplase or placebo, the 30-day mortality was 7.2% compared with 9.8% in controls, a reduction of 27% by alteplase. In another trial, 721 patients were randomized to placebo or alteplase; all patients received acetylsalicylic acid and intravenous heparin. The 14-day mortality was only 2.8% in the alteplase group, 51% less than that in the control group. It is most important that the favorable impact on hospital survival be maintained at 1 year for any thrombolytic drug. Large-scale trials directly comparing mortality after alteplase, streptokinase, or anistreplase are being performed or are in the planning phase. The risk of bleeding exists with any thrombolytic agent; intracranial bleeding is the most serious risk. In a large trial in 5,011 patients with acute myocardial infarction, stroke occurred in 1.1% of alteplase-treated patients compared with 1.0% in placebo-treated controls. Haunting problems are residual stenosis of the coronary artery and reocclusion. Urgent angioplasty does not seem to be the right answer; more effective antithrombotic strategies have yet to be developed.
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PMID:Thrombolytic treatment in acute myocardial infarction. 211 32

The effects of isradipine, a new dihydropyridine calcium antagonist, were evaluated in 24 patients referred for elective cardiac catheterization because of suspected coronary artery disease. Hemodynamics and left ventricular (LV) function (by digital subtraction angiography) were measured at baseline and during rapid atrial pacing (mean peak heart rate 135 beats/min), which induced chest pain or electrocardiographic changes in all patients. After a control pacing period, intravenous isradipine (0.01 mg/kg, n = 16) or placebo (n = 8) was administered in a double-blind fashion and all variables were measured again at baseline and during pacing to the same maximum heart rate. Before isradipine was given, pacing had no effect on systolic blood pressure, while increasing diastolic blood pressure (68 +/- 8 to 87 +/- 11 mm Hg, p less than 0.0001) and LV end-diastolic pressure measured in the immediate postpacing period (13 +/- 5 to 18 +/- 6 mm Hg, p less than 0.03) and decreasing LV end-diastolic volume index (59 +/- 18 to 40 +/- 12 ml/m2, p less than 0.001), stroke volume index (37 +/- 11 to 23 +/- 10 ml/m2, p less than 0.0001), ejection fraction (0.64 +/- 0.07 to 0.53 +/- 0.12, p less than 0.0003) and percent regional shortening in 4 of 5 myocardial wall segments. During pacing after isradipine, systolic and diastolic blood pressures were lower, ejection fraction was higher and percent regional shortening decreased in only 2 of 5 myocardial segments. In comparison to placebo, isradipine increased baseline heart rate, ejection fraction and stroke volume index while it decreased arterial pressure and end-systolic volume index before the second pacing period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous isradipine on left ventricular performance during rapid atrial pacing in coronary artery disease. 213 68

The prognostic factors in the acute stage of 893 myocardial infarction patients, admitted during a period from 1970 to 1986, were analysed. The overall mortality was 15.6%, including 14.4% cardiac death and 1.1% non-cardiac death. Single factor analysis indicated that age, sex, occupation, history of hypertension, chest pain during the episode, systolic blood pressure, heart rate and site of infarction at the time of admission, presence of complications such as cardiogenic shock, arrhythmias, stroke and monitoring in CCU or not were related to the overall mortality and cardiac death. Multiple factor logistic regression analysis indicated that for the overall mortality, the independent prognostic factors included presence of cardiogenic shock, heart rate and chest pain at the time of admission; for the cardiac death, the independent factors included age, occupation, history of hypertension, heart rate and chest pain at the time of admission, involvement of anterior wall and presence of cardiogenic shock and arrhythmias. Basing on the above findings we establish a risk factors predicting prognostic model of acute myocardial infarction in its acute stage.
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PMID:[Prognostic factors in the acute stage of myocardial infarction: analysis of 893 cases]. 220 38

The acute haemodynamic effects of intravenous infusion of adenosine, a dilator of most vascular beds, were studied in 16 patients (seven with coronary artery disease, nine with normal coronary arteries) undergoing cardiac catheterization for investigation of chest pain. At the lowest dose used (4.3 mg min-1) adenosine increased minute ventilation by 44% (P less than 0.01, n = 11) and reduced pulmonary vascular resistance by 20% (P less than 0.05) without causing other significant haemodynamic changes. Symptoms, including chest discomfort in 14 patients and dyspnoea in 11, limited the maximum dose to 8.5 +/- 2.3 mg min-1 (mean +/- SD, 108 +/- 24 micrograms kg-1 min-1). At this dose, adenosine reduced pulmonary and systemic vascular resistance (by 38% and 34%, respectively) and increased heart rate (by 34%), stroke index (by 12%) and cardiac index (by 52%). Systemic blood pressure and right atrial pressure did not change. Unexpectedly, adenosine increased left ventricular end-diastolic pressure (LVEDP) (from 5 +/- 6 to 14 +/- 10 mmHg, n = 8), pulmonary capillary wedge pressure (from 3 +/- 2 to 10 +/- 5 mmHg, n = 16) and consequently mean pulmonary artery pressure (from 10 +/- 2 to 16 +/- 5 mmHg). Minute ventilation increased by 84% (n = 11), resulting in hypocapnia (PCO2: 31 +/- 3 mmHg, n = 8) and alkalosis (pH: 7.46 +/- 0.02, n = 8). Oxygen consumption was unchanged during the infusion, but increased by 21% 5 min post infusion. All effects were similar in patients with and without coronary artery disease. Adenosine therefore causes pulmonary and systemic vasodilation and respiratory stimulation. Symptoms and an increase in LVEDP of uncertain cause, which occur with high doses, may limit the use of adenosine as a systemic vasodilator in conscious subjects. However at lower doses adenosine causes selective pulmonary vasodilation which merits further study.
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PMID:Acute haemodynamic effects of intravenous infusion of adenosine in conscious man. 228 21


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