Biomedical subjects

J Elsperger

Publications and source records attributed to J Elsperger.

7 recordsLinked to original sources

PubMed1988

Increasing precordial QRS voltage correlates with improvement in left ventricular function following anterior myocardial infarction.

To evaluate whether changes in QRS voltage reflect changes in left ventricular function after myocardial infarction, 28 patients were studied following anterior myocardial infarction. Two-dimensional echocardiograms and 12-lead electrocardiograms were obtained during the acute phase of the infarction and again after at least 30 days of recovery (mean, 8 +/- 8 months). At follow-up, 11 patients (group A) showed improvement in left ventricular systolic function; 9 had increased net QRS voltage in V1-6 and 8 in V1-4. No improvement in ventricular function was found in 17 patients (group B); 7 had increased QRS voltage in V1-6 (p less than 0.05 vs group A) and only 5 in V1-4 (p less than 0.05 vs group A). For detection of improved left ventricular function, the sensitivity, specificity, and predictive value of the change in net QRS voltage for leads V1-6 was 82%, 59%, and 56% respectively, and for leads V1-4 was 73%, 71%, and 62% respectively. Neither R wave voltage, Q wave voltage, nor the total number of Q waves was reliable for identifying patients with improving left ventricular function. Thus, increasing net QRS voltage in the precordial electrocardiographic leads during long-term follow-up after anterior myocardial infarction correlates with and has a reasonable sensitivity for detection of improvement in left ventricular systolic performance.

Adult↗

PubMed1988

Echocardiography performed by emergency physicians: impact on diagnosis and therapy.

Echocardiography is the "gold standard" for diagnosing many cardiac and pericardial abnormalities. It is noninvasive and accurate, but in most emergency departments is only as available as the technician or the cardiologist. We describe our experience in training emergency physicians to perform cardiac ultrasound, and clinical situations in which we have found echocardiography to be useful.

Adolescent↗

PubMed1988

Reduced lipid peroxidation in dilated hearts of cardiomyopathic turkeys.

Adverse pulmonary reactions to some nitrofuran antibiotics are thought, in part, to involve production of reactive oxygen radicals. Furazolidone, a nitrofuran antibiotic, causes a dilated cardiomyopathy in domestic turkeys. The mechanism of this drug induced cardiomyopathy is unknown. We investigated the possible role of free radical injury in this heart failure model. Left ventricular lipid peroxidation capacity, assessed by two methods (the thiobarbituric acid reactive substances and lipid hydroperoxides assays respectively), was investigated in five 5-8 week old cardiomyopathic turkeys with severe cardiac dilatation, left ventricular dysfunction and systemic hypotension, and in five control birds. Superoxide dismutase activity, total and manganese, was also measured in the crude left ventricular homogenates. Both lipid peroxidation products were reduced in the myopathic hearts: thiobarbituric acid reactive substances (malondialdehyde) 70(SEM 4) v 86(3) nmol.100 mg protein-1 in controls, p less than 0.02; and lipid hydroperoxides 29(7) v 74(14) nmol.100 mg protein-1, p less than 0.02. Total superoxide dismutase activity was similar in cardiomyopathic and control hearts: 670(26) v 657(105) nitrite units.100 mg protein-1. Although total superoxide dismutase activity was unchanged, we found decreased manganese superoxide dismutase in the dilated hearts compared with controls (54% v 84% of total activity, p less than 0.02). In separate in vitro experiments furazolidone (2-10 mg.g wet weight-1) did not increase malondialdehyde production in turkey (or rat) left ventricular homogenates. These results indicate that cardiomyopathy induced by furazolidone is associated with decreased myocardial lipid peroxidation. Although as yet unexplained, the decrease may be due to a diminished amount of heart lipid susceptible to peroxidation accompanying the process of cardiac hypertrophy and dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Acute Disease↗

PubMed1987

Beta-adrenergic function in a congestive cardiomyopathy model.

We investigated the cardiac beta-adrenergic-adenylate cyclase (AC) system in turkeys inbred for congestive cardiomyopathy (CCM) and the relation of this system to echocardiographically determined left ventricular shortening fraction (LVSF) in individual 56-day-old birds. The isoproterenol (Iso)-stimulated, NaF-stimulated, and basal AC activities in CCM birds were decreased to 69, 72, and 86%, respectively, of control values, P less than 0.05. By linear regression analysis there was significant direct correlation of initial LVSF in CCM birds with each of the following: change in heart rate (HR) after Iso function; Iso-stimulated, NaF-stimulated, and basal AC activities, and density of beta-adrenergic receptors. In addition, we investigated the effect of Iso infusion (0.4 microgram X kg-1 X min-1) on systemic hemodynamics. In CCM birds the initial LVSF was 72% of the control value, P less than 0.01; the initial HR was 112% of the control value, P less than 0.01. During Iso infusion both the LVSF and HR in control birds were increased, whereas in CCM turkeys with marked cardiac dilatation neither of these parameters changed. In 10-day-old CCM turkeys, which show no cardiac dilatation, NaF-stimulated AC activity was reduced to 70% of the control values, whereas basal and Iso-stimulated AC activities were unchanged. Thus an abnormality in the beta-adrenergic-adenylate cyclase system is present in CCM birds before development of cardiac dilatation; when cardiac dilatation is severe, a global defect in this system can be directly related to depressed inotropic and chronotropic responsiveness to Iso infusion in individual turkeys.

Adenylyl Cyclases↗

PubMed1984

Embolic potential of left ventricular thrombi detected by two-dimensional echocardiography.

We sought to determine whether an association existed between the echocardiographic appearance of left ventricular thrombi and systemic embolization. We reviewed the clinical and echocardiographic characteristics of 60 patients who underwent diagnostic two-dimensional echocardiography for left ventricular thrombi. Sixteen of these 60 patients (27%) had evidence of systemic embolization. Multiple echocardiographic characteristics of left ventricular thrombi were analyzed, including mobility, shape, heterogeneity, echo density, layering, central echo lucency, presence within an aneurysm, and association with low-density swirling echoes. Incidence of embolization was significantly higher in patients with thrombi that were mobile or protruded into the left ventricular cavity (p less than .002 and p less than .05, respectively). Bayesian analysis indicated that the pretest likelihood for embolization was 27% and increased in the presence of mobility, central echo lucency, and protrusion to 60%, 50%, and 40%, respectively. A stepwise regression indicated that mobility was the first and protrusion the second most helpful echocardiographic characteristic in identifying patients with embolic phenomena. Clinical features were of less help in identifying the risk for embolization of patients with left ventricular thrombi. Nine of 31 patients (29%) with recent myocardial infarction (less than 3 weeks) has emboli in contrast to five of 26 patients (19%) with remote myocardial infarction (greater than 3 weeks) (p = NS). The three patients without infarction had congestive cardiomyopathy and two had emboli.

Echocardiography↗

PubMed1981

Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography.

To study the incidence of left-ventricular thrombosis after transmural myocardial infarction, we performed serial two-dimensional echocardiography in 70 consecutive patients. Thirty-five patients had inferior-wall infarction: none had a left-ventricular thrombus. The other 35 had anterior-wall infarction: 12 had left-ventricular thrombi. Thrombi were diagnosed an average of five days after the infarction (range, one to 11 days). All patients with left-ventricular thrombi had severe apical-wall-motion abnormalities (akinesis or dyskinesis). Twenty-six of the 35 patients with anterior infarctions had apical akinesis or dyskinesis on echocardiography; left-ventricular thrombi developed in 12 of these 26 (46 per cent). We conclude that patients with severe apical-wall-motion abnormalities during acute transmural anterior myocardial infarction are at high risk for left-ventricular thrombosis. This high-risk group can be identified before the development of left-ventricular thrombi. Patients with inferior infarction or anterior infarction without a severe apical-wall-motion abnormality are at low risk.

Adult↗