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Biomedical subjects

H S Mueller

Publications and source records attributed to H S Mueller.

At least 55 records · Page 3Linked to original sources
PubMed1980

Sequential thallium-201 myocardial scintigraphy after acute infarction in man: comparison to creatine kinase-MB release pattern.

Three sequential Tl-201 myocardial perfusion studies were performed in 21 patients (18 men, 3 women) with first acute transmural myocardial infarction. The Tl-201 image defect size was determined with a semiquantitative visual scoring method and temporal changes in image defect size were compared to CK-MB infarct size and enzymatic evidence of progressive myocardial necrosis and infarct extension. Progressive decreases in Tl-201 image defect size were observed and the visual score in all 21 patients decreased significantly from 6.5 +/- 3.7 (mean +/- SD) on day 1 to 4.9 +/- 3.5 on day 12. Eleven patients without evidence of infarct extension had significantly lower infarct size, a significant decrease in visual score by the 12th day and had significantly smaller Tl-201 defects at all three study times compared to 10 patients with infarct extension. Seven of 10 (70%) with extension had an initial score greater than or equal to 7 compared to only 2/11 (18%) without extension. The temporal behavior of Tl-201 image defects is related to the size of the infarction and presence or absence of extension. Sequential studies comparing early initial and subsequent defect size may assist in evaluating the behavior of ischemic and infarcted myocardium in the postinfarction period.

Acute Disease↗
PubMed1980

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Plasma 1-norepinephrine and epinephrine contents were strikingly elevated in 70 patients during evolution of myocardial infarction. Propranolol or placebo, 0.1 mg/kg i.v., was administered randomly an average of 10 h after infarction and continued orally for 3 d. Propranolol, but not placebo, acutely decreased 1-norepinephrine contents from 2.24 +/- 1.33 (mean +/- SD) to 1.31 +/- 0.74 microgram/liter, P less than 0.001, and epinephrine contents from 0.97 +/- 0.42 to 0.74 +/- 0.42 microgram/liter, P less than 0.02. Decreases in 1-norepinephrine contents were related to the initial plasma concentrations, r = 0.85, P less than 0.001. A similar, but less strong relationship was observed between the initial epinephrine contents and propranolol-induced changes, r = -0.51, P less than 0.01. Propranolol reduced plasma-free fatty acid contents from 1,121 +/- 315 to 943 +/- 274 mumol/liter, P less than 0.001. Decreases in plasma contents of free fatty acids were related to decreases in epinephrine, r = 0.66, P less than 0.001. Propranolol did not cause significant additional changes in plasma catecholamine contents during the subsequent 3 d. In the placebo group 1-norepinephrine contents had decreased 24 h after infarction from 1.92 +/- 0.99 to 1.37 +/- 0.93 microgram/liter, P less than 0.02. Plasma epinephrine contents did not change. Heart rate remained below the control values during the entire study period in the propranolol, but increased in the placebo group. The data indicate that sympathetic hyperactivity, indirectly reflected by plasma catecholamine contents, is acutely reduced by propranolol during evolution of myocardial infarction.

Adult↗
PubMed1980

Clinical estimation of infarct size by 201thallium perfusion scintigraphy and by creatine kinase-MB in early myocardial infarction.

201Thallium (201Tl) perfusion scintigraphy was performed in 22 patients with first acute transmural myocardial infarction within the initial 12 h after onset of symptoms. The size of the abnormally perfused area on 201Tl images was estimated by visual analysis and by a computer-assisted technique. 201Tl values for infarct size were compared to a biochemical estimate of infarct size using the cardiac specific esoenzyme creatine kinase-MB (CK-MB) and total creatine kinase (CK). Estimates of myocardial damage obtained from the visual and computer-assisted analysis of the 201Tl images showed a statistically significant correlation with the enzymatic estimates of infarct size. These results suggest that quantitative evaluation of 201Tl image defects may provide useful information regarding the degree of myocardial damage in the very early stages of acute infarction before biochemical estimates of infarct size are available, and that sequential imaging with 201Tl might provide an independent method of monitoring evolutionary changes in myocardial damage.

Adult↗
PubMed1978

Effects of dopamine on haemodynamics and myocardial energetics in man: comparison with effects of isoprenaline and L-noradrenaline.

The effects of dopamine (DOPA) on haemodynamics, coronary blood flow and myocardial oxygen requirements were compared with those of L-noradrenaline and isoprenaline (isoproterenol) in patients after open-heart surgery, performed because of mitral valvular and congenital heart disease. The patients were in low cardiac output state but not in shock. DOPA increased heart rate less than isoprenaline, averaging 22 and 31 beats/min, and was less arrhythmogenic. DOPA increased mean arterial pressure by an average of 7 mmHg, whereas isoprenaline had little effect; noradrenaline uniformly increased all measurements of arterial pressure. DOPA and isoprenaline increased cardiac index by an average of 1.01 and 0.94 1 min--1 m--2; noradrenaline did not significantly improve peripheral perfusion. DOPA and isoprenaline decreased systemic vascular resistance by an average of 465 and 549 dynes s cm--5; noradrenaline increased resistance in all patients. For similar cardiac outputs average urine flow increased more with DOPA (75 ml/h) than with isoprenaline (28 ml/h). DOPA increased coronary blood flow and myocardial O2 consumption by an average of 28 and 3.60 ml min--1 100 g--1, noradrenaline by 16 and 1.93 and isoprenaline by 62 and 4.25 ml min--1 100 g--1 respectively. Arterial--coronary sinus O2 differences remained unchanged (normal) with DOPA and noradrenaline and decreased with isoprenaline on average by 1.10 ml/100 ml. Myocardial lactate utilization was normal before and during catecholamine administration. It is concluded that, in its haemodynamic effects, DOPA is intermediate between noradrenaline and isoprenaline. The effects of DOPA on coronary blood flow and myocardial O2 consumption are closer to those of noradrenaline than of isoprenaline. DOPA increase coronary blood flow according to myocardial metabolic demand; it is not a potent primary coronary vasodilator. DOPA, although increasing myocardial O2 consumption more than noradrenaline, is by far less O2-demanding than isoprenaline. DOPA appears to be the superior vasoactive agent among the three catecholamines for the treatment of low cardiac output state in patients with preserved coronary reserve.

Adult↗
PubMed1978

Diagnosis of coronary artery disease with 201Tl. Computer analysis of myocardial perfusion images.

The diagnostic sensitivity of visually interpreted and computer-analyzed 201Tl myocardial perfusion images was compared to that of exercise electrocardiograms in 8 angiographically normal subjects and 24 patients with significant coronary artery disease. Visual interpretation was not significantly better than exercise ECGs. An index of perfusion homogeneity, derived from computer analysis of the 201Tl images, was more sensitive than visual interpretation (79% vs. 58%) and much more sensitive (p less than 0.05) than the exercise ECG (79% VS. 46%). The best overall sensitivity (88%) and specificity (75%) were achieved by combining computer analysis with exercise electrocardiography. The computer also permits enhanced detection of subtle perfusion changes which may not seem significant to the eye.

Computers↗
PubMed1978

Effect of dopamine on hemodynamics and myocardial metabolism in shock following acute myocardial infarction in man.

Eight patients in shock associated with acute myocardial infarctions were treated with dopamine. We titrated the dopamine dose to increase mean arterial pressure to 65-70 mm Hg and urine output to greater than 40 ml/hr. Increase of heart rate to 120-125 beats/min and occurrence of potentially dangerous arrhythmias were limiting end-points. Dopamine administration averaged 17.2 microgram/kg/min. Heart rate increased from 95 to 118 beats/min (P less than 0.001), and mean arterial pressure rose from 60 to 65 mm Hg (P less than 0.05). Dopamine increased myocardial contractility as indicated by increase in cardiac index and systolic ejection rate, with only moderate decrease in systemic vascular resistance. Pulmonary wedge pressure and right atrial pressure decreased from 23 to 18 mm Hg (P less than 0.05) and from 10 to 8 mm Hg (P less than 0.001) respectively. Improvement in hemodynamic status by dopamine was associated with deterioration of myocardial metabolism. Myocardial oxygen extraction ratios and arterial-coronary sinus oxygen differences increased from 73 to 76% (P less than 0.05) and from 13.02 to 14.19 ml/100 ml (P less than 0.02) respectively. Myocardial lactate production increased from -8 to -15% (P = 0.05). We conclude that dopamine improved cardiac performance at the expense of myocardial oxygenation and that dopamine is potentially harmful to acutely ischemic myocardium.

Acute Disease↗