Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The National Blood Pressure Study (NBPS) is a single blind trial designed to test the efficacy of active drug treatment in reducing complications from mild hypertension (mean diastolic pressure = 95-109 mmHg). 2. Between 1973 and 1975, four centres screened about 104 000 subjects aged 30-69 years, yielding an estimated prevalence of hypertension (greater than or equal to 95 mmHg diastolic) of 16% and of moderate-to-severe hypertension (greater than of equal to 110 mmHg diastolic) of 1-3%. 3. Some 4000 subjects selected for untreated uncomplicated mild hypertension were randomized to either active treatment (cholorothiazide +alpha-methyldopa and/or a beta-adrenoreceptor antagonist as required) or to matching placebos. 4. At 1 year mean pressures had fallen significantly below entry pressures in both groups but in the active group the fall was greater by a margin of 14-4+/-1-3 (SEM) mmHg systolic and 7-1+/-0-7 mmHg diastolic. At 1 year 5% of subjects in the placebo group had been placed on active treatment on the ethical grounds that pressure had exceeded the mild hypertension limit. 5. Trial end-points (death, morbidity from stroke, hypertensive heart and renal disease, and ischaemic heart disease) number 106 (nine deaths) thus far, of which ischaemic heart disease accounts for 71% and stroke 19%. 6. The duration of trial may need to be extended beyond the original estimate of 5 years.
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PMID:Report on progress in the Australian National Blood Pressure Study (NBPS). 107 98

To determine the effects of myocardial revascularization on decreased left ventricular diastolic compliance consequent to chronic stable coronary artery disease, 15 patients with patent coronary artery bypass grafts (Group I) were compared with 8 patients with occluded grafts (Group II) studied before and after operation. In addition, eight normal patients served as controls. Left ventricular diastolic compliance was assessed by: (1) total observed diastolic compliance: stroke volume (V) related to left ventricular diastolic pressure (P) change (deltaV/deltaP) normalized for end-systolic volume; (2) left ventricular stiffness index of passive elastic modulus (a equals slope of deltaP/deltaV related to mean left ventricular diastolic pressure); and (3) fractional pattern of left ventricular filling. All patients had normal sinus rhythm and none had preoperative or postoperative mitral regurgitation. The two groups with coronary disease were well matched preoperatively for ventricular function, volumes, mass, segmental contraction and compliance. Ejection fraction increased in Group I (0.56 preoperatively to 0.65 postoperatively, P less than 0.05) but was unchanged in Group II (0.63 To 0.61, P greater 0.05). Postoperative indexes of left ventricular compliance improved in Group I: (1) 0.110 to 0.150 (P less 0.05); (2) 0.030 TO 0.019 (P less 0.05); and (3) 37 to 30 percent filling during last one third of diastole (P less 0.05). These indexes were unchanged postoperatively in Group II: (1) 0.109 to 0.102 (P greater 0.05); (2) 0.033 to 0.039 (P greater than 0.05); and (3) 36 to 41 percent (P greater 0.05). Compliance indexes were not altered (P greater 0.05) in a subset of seven patients in Group I with preoperative or intercurrent myocardial infarction. Thus, this investigation demonstrates the relatively reversible nature of abnormal left ventricular compliance after successful coronary artery bypass surgery in certain patients with ischemic heart disease.
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PMID:Improvement of reduced left ventricular diastolic compliance in ischemic heart disease after successful coronary artery bypass surgery. 107 48

Left ventricular function was studied in 17 patients with ischaemic heart disease and compared with 4 patients with normal left ventricular function. The patients in the homogeneous group of ischaemic heart disease were further subdivided into those 'without angina' (n=5) and those 'with angina' (n=12), depending upon the presence of angina during supine leg exercise at the time of definitive study. At rest there was no significant difference in the heart rate, cardiac output, stroke volume, and left ventricular end-diastolic pressure (LVEDP) in the three groups. During exercise the cardiac output and stroke volume were significantly depressed and LVEDP was significantly raised in the ischaemic heart disease group as a whole but within this group failed to show any significant difference in patients with and without angina. The left ventricular end-diastolic volume (LVEDV) and end-systolic volume (LVESV) measurements showed clear separation of these three groups only on exercise. On exercise, there was decrease in LVEDV and LVESV (P less than 0.05; P less than 0.02) in the group with normal left ventricular function, no change in the group with ischaemic heart disease without angina, and striking increase in LVEDV and LVESV in the group with ischaemic heart disease and angina (P less than 0.01 and P less than 0.02, respectively). This angiographic method of assessing left ventricular function shows clear separation of the three groups and also highlights the significance of angina. Ejection fraction (EF), a commonly measured parameter of left ventricular function, failed to reflect consistent changes on exercise as compared to values at rest which emphasizes the limitations of the measurement of ejection fraction at rest.
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PMID:Left ventricular angiography on exercise. A new method of assessing left ventricular function in ischaemic heart disease. 108 66

To study the efficacy of isosorbide dinitrate in prevention of myocardial ischemia, 20 patients with angiographically proved coronary artery disease underwent atrial pacing (mean rate 138/min) before (P1), 10 minutes after (P2) and 65 minutes after (P3) sublingual administration of 5 mg of isosorbide dinitrate. The symptomatic, hemodynamic and metabolic responses were evaluated at rest and during each pacing period. Angina occurred in all subjects during P1. Angina did not recur or was less severe in 17 of 19 patients during P2 and in 19 of 20 patients during P3. Resting left ventricular end-diastolic pressure for the group was normal at 11 plus or minus 4 mm Hg (mean plus or minus standard deviation). On interruption of pacing at 4.5 minutes during P1, average end-diastolic pressure during sinus rhythm was abnormal (18 plus or minus 6 mm Hg). After administration of isosorbide dinitrate mean left ventricular end-diastolic pressure was significantly decreased at rest and remained normal when pacing was interrupted during P2 and P3. Brachial arterial pressure, cardiac index, tension-time index, left ventricular stroke work index and maximal rate of rise of left ventricular pressure were all diminished at rest before and during P2 and P3. S-T segment depression was less during P2 and P3 than during P1. Before isosorbide dinitrate was given, resting myocardial lactate extraction was 15 plus or minus 11 percent during P1 lactate extraction decreased to minus2 plus or minus 25 percent. Lactate extraction was significantly greater during P2 and P3 than during P1. This study demonstrates that sublingual administration of 5 mg of isosorbide dinitrate has a significant protective effect against pacing-induced myocardial ischemia at 10 and 65 minutes after administration.
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PMID:Effects of isosorbide dinitrate on the response to atrial pacing in coronary heart disease. 115 42

The left ventricular end-diastolic volume (EDV), end-systolic volume (ESV) and systolic ejection fraction (SV/EDV) were determined in 6 healthy subjects, 21 patients with ischemic heart disease and 8 patients with mitral stenosis by the left ventricular 133Xe washout technique. Cardiac and stroke indexes as well as left ventricular work and stroke work indexes do not differ in all three groups. A significantly higher EDV and ESV together with a low SV/EDV suggested impaired left ventricular function in patients with ischemic heart disease.
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PMID:Left ventricular end-diastolic volume in advanced ischemic heart disease; comparison between healthy subjects and patients with mitral stenosis. 118 18

N-Dimethylisopropyl propranolol (DMP) is a quaternary derivative which lacks significant beta-adrenergic blocking and local anesthetic effects. It has been reported, nonetheless, to be effective in treating experimental arrhythmias and in limiting the extent of ST-segment elevations following experimental coronary occlusion. The present study examined the effects of DMP on the hemodynamics and myocardial oxygen demands of anesthetized dogs. After a single dose of 3 mg/kg, heart rate fell from 146 +/- 8 to 124 +/- 6 beats/min (P less than 0.0025), and aortic systolic pressure fell from 151 +/- 11 to 141 +/- 9 mm Hg (0.05 less than P less than 0.10), resulting in a 16.8% reduction in the tension-time index. Stroke volume was reduced by 10% despite a 54% increase in left ventricular end-diastolic pressure, suggesting a negative inotropic effect. This was supported by a decrease in maximum extrapolated contractile element velocity from 9.10 +/- 1.05 to 6.61 +/- 65 units/sec (P less than 0.0025). Myocardial oxygen consumption was reduced from 12.0 +/- 1.4 to 9.9 +/- 1.5 ml/min/100 g tissue (P less than 0.05). Myocardial oxygen extraction was unchanged, indicating that the decrease in oxygen consumption resulted from a reduction in myocardial oxygen demand. When heart rate and systolic pressure were artificially restored to control levels, after the administration of DMP, myocardial oxygen consumption remained significantly below the control level. DMP, therefore, appeared to reduce myocardial oxygen demands primarily by its negative inotropic effect. This drug may have application in the treatment of ischemic heart disease.
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PMID:N-dimethylisopropyl propranolol. Effects on myocardial oxygen demands. 124 83

The effects of methylprednisolong treatment on acute myocardial ischemia were studied in nine closed chest dogs. After 1 hour of proximal occlusion of the left anterior descending coronary artery, an intravenous bolus injection (50 mg/kg body weight) of methylprednisolone was administered and its effects studied during an additional 2 hours of occlusion. After 2 hours of treatment the following significant mean alterations from levels after 1 hour of occlusion were noted: an increase of 16.7% in heart rate and decreases of 23% in left ventricular end-diastolic pressure, 32% in stroke volume, 14% in cardiac output and 37% in stroke work. Peak systolic pressure, maximal rate of rise of left ventricular pressure (dP/dt), left ventricular end-diastolic volume, systemic vascular resistance and coronary sinus blood flow changed less than 10%. Ejection fraction and regional cardiac wall motion were not improved. Metabolic dysfunction of the coronary-occluded myocardium, revealed by regional lactate as well as potassium derangements, persisted throughout the 2 hour treatment period. Comparison of these results with equivalent data from an untreated series of nine dogs with 3 hours of occlusion demonstrated no improvement in the treated series. Methylprednistone failed to restore regional cardiac metabolic and mechanical function, and treatment was associated with a further rise in S-T segment elevations. Administration of methylprednisolone after 1 hour of proximal left anterior descending coronary occlusion apparently does not reverse cardiac dysfunction in the first 2 hours of treatment.
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PMID:Methylprednisolone treatment in acute myocardial infarction. Effect on regional and global myocardial function. 125 94

We studied whether cardiac abnormalities contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation (NVAF). M-mode and 2D echocardiography were performed in four age- and gender-matched groups: 20 stroke patients with NVAF, 20 patients with NVAF who had not suffered a previous stroke, 20 stroke patients with sinus rhythm, and 40 healthy controls. Their mean age was 77 years. The two groups with atrial fibrillation differed from healthy controls in that they had more 2D-echocardiographic findings of severe left-ventricular-wall-motion abnormalities (p < 0.05) and tended more often to have enlarged left ventricles, and hypertrophic and congestive cardiomyopathy. Left atrial diameter was 47 mm compared to 41 and 39 mm in the two groups with sinus rhythm (p < 0.001). Intracardiac thrombi were only found in the two atrial-fibrillation groups (with stroke: 15% without stroke: 5%). Aortic sclerosis was common in all groups (30-60%), as was mitral annulus calcification (10-20%). The only significant difference between the two atrial-fibrillation groups was a higher frequency of earlier ischemic heart disease in the stroke group. Both atrial-fibrillation groups had cardiac abnormalities predisposing for embolic as well as thrombotic stroke.
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PMID:Echocardiographic findings and the increased risk of stroke in nonvalvular atrial fibrillation. 130 Dec 43

Forty-six patients with ischemic heart disease with considerable dysfunction of the myocardium were subjected before operation of aortocoronary shunting to veloergometry with calculation of indices of the central hemodynamics by the method of tetrapolar rheoplethysmography, echocardioscopy before and after taking nitroglycerin. Close interrelation was noted between the increase of the stroke volume during veloergometry, increased fraction of output after taking nitroglycerin and improved contractile capacity of the myocardium after aortocoronary shunting.
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PMID:[The prognostic assessment of the reversibility of myocardial dysfunction in patients with ischemic heart disease after aortocoronary bypass]. 130 70

Technetium-99m pertechnetate equilibrium ventriculography was used to evaluate the effects of captopril in a single dose of 50 mg on the changes in ST segment depression during the identical bicycle ergometer exercise, as well as on systemic and regional hemodynamic parameters in 10 patients (mean age 52 years) with Functional Classes II-III exercise-induced angina pectoris. During exercise performed 45 and 90 minutes after captopril, ST segment depression decreased by 30 +/- 0 (p less than 0.05), and 32 +/- 10% (p less than 0.02), respectively as compared to baseline ST segment displacement. Following 90 minutes after the drug administration, end-systolic volume reduced both at rest and during exercise, resting stroke volume increased from 71 +/- 4 to 76 +/- 4 ml (p less than 0.01), whereas exercise stroke volume rose from 69 +/- 3 to 74 +/- 3 ml (p less than 0.03); with the drug, ejection fraction showed a 5% increase (p less than 0.02) at rest and a 4% increase (p less than 0.02) on exercise. Thus, captopril had a beneficial effect on the hemodynamics and reduced myocardial ischemia in patients with exercise induced angina.
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PMID:[Effect of captopril on myocardial ischemia, intracardiac hemodynamics and regional left-ventricular contractility in patients with stenocardia]. 131 15


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