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Biomedical subjects

H G Olson

Publications and source records attributed to H G Olson.

33 records · Page 2Linked to original sources
PubMed1980

Technetium-99m stannous pyrophosphate myocardial scintigrams in pericardial disease.

Technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams were obtained in 35 acute pericarditis and in three chronic constrictive pericarditis patients. Thirteen of 35 acute pericarditis patients (37%) and one of three chronic constrictive pericarditis patients (33%) had abnormal scintigrams (a diffuse pattern in eight patients and a regional pattern in six patients). Of the 17 acute pericarditis patients with classic ST-segment changes of acute pericarditis, 10 (56%) had abnormal scintigrams compared to three of 17 patients (18%) without these ECG changes (P less than 0.02). These data indicate that pericardial disease may cause an abnormal scintigram. Therefore, one must rule out pericardial disease before concluding that a positive scintigram is due to acute myocardial infarction.

Acute Disease↗
PubMed1980

Sensitivity and specificity of Tc-99m-pyrophosphate myocardial scintigraphy for the detection of acute myocardial infarction.

Tc-99m-pyrophosphate myocardial scintigraphy was performed on 1,077 patients admitted to the Coronary Care Unit. Results of scintigraphy were compared to the diagnosis as established by ECG, enzymes, and clinical findings to determine the sensitivity and specificity of scintigraphy for the diagnosis of acute myocardial infarction (AMI). Scintigrams were graded according to the intensity of myocardial radioactivity and the distribution pattern of activity as either diffuse or localized. In a coronary care unit, a scintigram of positive intensity grade is 92% sensitive and 68% specific for the diagnosis for AMI. A localized pattern of myocardial radioactivity is 66% sensitive and 93% specific for AMI. With a localized pattern of the highest intensity, the sensitivity is 28% with a specificity of 99.8% for AMI. Therefore, a myocardial scintigram of normal intensity grade excludes the diagnosis of AMI with a 92% probability. A localized pattern is a strong indicator of an AMI and a localized pattern of the greatest intensity is very specific for AMI.

Acute Disease↗
PubMed1979

Prognostic value of a persistently positive technetium-99m stannous pyrophosphate myocardial scintigram after myocardial infarction.

Technetium-99m stannous pyrophosphate myocardial scintigrams were obtained in 138 clinically stable patients 32.7 +/- 47.3 weeks (range 6 to 260) after acute myocardial infarction. Of the 138 patients, 74 (54 percent) had a persistently positive scintigram. Patients with such a scintigram were more likely to have severe angina pectoris, compensated congestive heart failure, anterior location of acute myocardial infarction, Q waves and S-T segment elevation in the electrocardiograms, cardiomegaly, left ventricular dyssynergy (dyskinesia or global dyssynergy), and an ejection fraction of less than 50 percent. During a follow-up period of 11.6 +/- 6.9 months after scintigraphy, 42 percent of the patients with a persistently positive scintigram had either a cardiac death, a nonfatal myocardial infarction, unstable angina pectoris or decompensated congestive heart failure compared with 13 percent of the patients with a negative scintigram (P less than 0.001). Of the 14 patients with cardiac death, 13 (93 percent) had a persistently positive scintigram. A persistently positive scintigram not only was the best single predictor of cardiac death and combined end points, but also added significantly to the predictive ability of the other clinical variables, including age, location of acute myocardial infarct, clinical status, electrocardiographic findings, and chest X-ray findings. It is concluded that technetium-99m stannous pyrophosphate myocardial scintigraphy has prognostic value in patients after acute myocardial infarction.

Adult↗
PubMed1979

Hemodynamics and echocardiograms before and after cardioversion of atrial fibrillation to normal sinus rhythm.

Hemodynamic and echocardiographic measurements were obtained in 15 patients prior to cardioversion and immediately, one, three, and five hours after cardioversion of atrial fibrillation to normal sinus rhythm. At five hours after cardioversion, there was improvement in cardiac index (P less than 0.005), in stroke index (P less than 0.005), and in stroke work index (P less than 0.025), but no significant change in heart rate, mean pulmonary capillary wedge pressure, left atrial dimemsions (LAD), left ventricular end-diastolic dimensions (LVEDD), or left ventricular end-systolic dimension (LVESD). At follow-up one week to nine months after cardioversion, 10 of the 15 patients (67 percent) remained in normal sinus rhythm. Neither the size of the left atrium, changes in hemodynamics, LAD, LVEDD, or LVESD, nor the presence or amplitude of the A-wave on the mitral valve echogram correlated with the persistence or normal sinus rhythm.

Adult↗
PubMed1978

Correlations of Tc-99m pyrophosphate myocardial scintigraphy and the results of coronary-artery bypass surgery.

This study indicates that abnormal myocardial scintigrams with Tc-99m pyrophosphate tend to improve after coronary-artery bypass surgery, frequently changing from positive to normal. The significance of this change is uncertain. It does not correlate well with the clinical state but may simply reflect the natural course of myocardial scintigraphy in response to hospitalization, medical management, and presumably improved myocardial oxygenation. Postoperative myocardial scintigrams are useful in detecting perioperative infarction. ECG interpretation may be difficult in the immediate postoperative period and, in three cases, there were scintigraphic criteria of perioperative infarction without diagnostic changes on ECG. Patients with positive preoperative scintigrams, especially in association with Functional Class IV angina, are at increased risk during coronary-artery bypass surgery.

Coronary Artery Bypass↗
PubMed1977

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.

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.

Acetylcholinesterase↗
PubMed1977

Follow-up technetium-99m stannous pyrophosphate myocardial scintigrams after acute myocardial infarction.

Technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams were obtained in 68 patients during acute myocardial infarction (AMI) and at follow-up 15.9 +/- 8.8 weeks later. All patients with AMI had a positive scintigram (2+ or greater); only one of 46 control patients (2%) had a positive (2+) scintigram. At follow-up scintigraphy 6 to 37 weeks following AMI, 57% of patients had a persistently positive scintigram even though recurrent AMI was suspected in only one of these patients. Patients with persistently positive scintigrams tended to have more severe disease as evidenced by compensated congested heart failure (41%) persistent angina (77%), and ECG evidence of ventricular dyssynergy (51%), We conclude that 1) in patients with prior AMI, a 2+ abnormality on 99mTc-PYP scintigram may not represent new AMI; 2) a persistently positive 99mTc- PYP scintigram may have prognostic implications since it occurs predominantly in patients with severe symptomatic coronary disease.

Acute Disease↗
PubMed1976

Pump dysfunction after myocardial infarction: importance of location, extent and pattern of abnormal left ventricular segmental contraction.

To delineate the relative effects on left ventricular function of the site, extent and nature of the abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression (P less than 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed (P less than 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial is largely the result of the more extensive area of necrosis rather than of the location of the infarction.

Adult↗
PubMed1975

Propranolol-withdrawal rebound phenomenon. Exacerbation of coronary events after abrupt cessation of antianginal therapy.

Effects on anginal symptoms of sudden withdrawal of large doses of propranolol or placebo were evaluated in 20 patients in a double-blind crossover efficacy trial requiring sudden cessation of the agent. With propranolol, 160 to 320 mg per day for six and 12 weeks, no patients had increased angina or nitroglycerin use, and there were no hospitalizations or deaths. However, within two weeks of discontinuance of propranolol, untoward ischemic events developed in 10 patients. Six had serious withdrawal complications: intermediate coronary syndrome in three, and ventricular tachycardia, fatal myocardial infarction, and sudden death in one each. In four patients discontinuance of placebo increased anginal symptoms; in the remaining 10, ischemic symptoms were not provoked. The rebound phenomenon was related to degree of pre-propranolol angina and relief of pain by the agent. Thus, chronically administered propranolol should be gradually reduced, and activity restricted during its withdrawal.

Adult↗
PubMed1975

Efficacy of beta adrenergic blockade in coronary heart disease: propranolol in angina pectoris.

Despite widespread clinical application of propranolol (P) in angina pectoris, convincing evidence of its efficacy has been incomplete, thereby resulting in continued controversy. Its antianginal effectivess was investigated in 20 patients with documented coronary heart disease in a 44-wk study incorporating a prolonged 12-wk lead-in period, individualization of P dosage in a 6-wk dose-finding period, and a 24-wk doule-blind crossover phase. On double-blind placebo, patients had 10.5 +/- 2.1 anginal attacks and consumed 12.8 +/- 3.0 nitroglycerin tablets (NTG) each week compared to 6.6 +/- 1.5 anginal episodes (- 37%, p less than 0.001) and 8.0 +/- 1.7 NTG (-38%, p less than 0.001) when on P. No patient experienced more angina with P than with placebo. In addition, time to onset of chest pain during treadmill exercise was prolonged by P from 190 +/- 16 to 248 +/- 22 sec (+31%, p less than 0.02) and ST depression was reduced from 1.7 +/- 0.21 to 0.99 +/- 0.18 mm (-42%, p less than 0.05). There was correlation (r = 0.64 p less than 0.01) between per cent declines in anginal frequency and resting double product with P. Thus, propranolol favorably altered several indices of myocardial ischemia in severe coronary heart disease. This investigation clearly documents the clinical efficacy of optimal beta adrenergic blockade in coronary disease and provides objective justification for the judicious application of propranolol in treatment of angina pectoris.

Adult↗