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Biomedical subjects

G D Plotnick

Publications and source records attributed to G D Plotnick.

At least 73 records · Page 4Linked to original sources
PubMed1983

Serum creatine kinase in the diagnosis of acute myocardial infarction. Optimal sampling frequency.

To document optimal sampling frequency, we reviewed creatine kinase (CK) myocardial specific isoenzyme (CKMB) results in 314 patients with suspected acute myocardial infarction (MI). In 127 patients with elevated CK/CKMB, peak CK observed using all samples (every four-hour [Q4hr] method) was compared with results that would have been obtained had samples been taken on admission and either twice daily (every 12-hour [Q12hr] method) or once daily (every 24-hour [Q24hr] method). Although average peak CK was statistically different (Q4hr greater than Q12hr greater than Q24hr), major underestimation of peak CK (greater than or equal to 500 units/L) was uncommon (3%) using the Q12hr method, suggesting that Q12hr sampling is a practical, cost-effective approach for patients with suspected acute MI.

Clinical Enzyme Tests↗
PubMed1983

Ventricular arrhythmias in patients with rest angina: correlation with ST segment changes and extent of coronary atherosclerosis.

Major ventricular arrhythmias occurring concurrently with myocardial ischemia are presumed to be the most frequent mechanism for sudden cardiac death. Two hundred eighteen catheterized patients with angina pectoris at rest were reviewed to identify clinical, ECG, and arteriographic features that might correlate with the presence of serious ventricular arrhythmias occurring during episodes of rest pain. Ventricular arrhythmias during episodes of rest pain were significantly more common in patients who manifested transient ST segment elevation in the anterior leads and in patients with marked transient ST segment shifts (greater than 5 mm). Ventricular arrhythmias during episodes of rest pain were not more common in patients with extensive coronary artery disease.

Angina Pectoris↗
PubMed1983

Acute changes in infranodal conduction time following left ventriculography and sublingual nitroglycerin administration in man.

During diagnostic cardiac catheterization for the evaluation of chest pain, His bundle electrograms were obtained in 32 male patients before and 2 to 5 minutes after each of two interventions known to acutely affect left ventricular volume and left ventricular end-diastolic pressure (the injection of 40 to 60 cc of contrast medium during left ventriculography and the administration of 0.4 mg of sublingual nitroglycerin). Changes in left ventricular end-diastolic pressure (18 +/- 6 vs 30 +/- 7 mm Hg, p less than 0.001 following ventriculography and 32 +/- 8 vs 19 +/- 8 mm Hg, p less than 0.005 following nitroglycerin administration) were accompanied by parallel alterations in HQ (48 +/- 8 vs 54 +/- 10 msec, p less than 0.005 following ventriculography and 57 +/- 10 vs 53 +/- msec, p less than 0.005 following nitroglycerin administration), but there were no significant changes in atrioventricular (AV) nodal conduction (AH). Significantly greater changes in HQ were seen in patients with triple-vessel coronary artery disease than in the remainder of the population, although there was clinical and/or ECG evidence of ischemia in only one patient. We conclude that factors other than progression of intrinsic conduction system disease may affect infranodal conduction. HQ should be interpreted cautiously in situations with rapidly changing hemodynamics, especially in patients with severe coronary artery disease.

Bundle of His↗
PubMed1983

Intrinsic sympathomimetic activity of pindolol. Evidence for interaction with pretreatment sympathetic tone.

Eighty-six hypertensive patients were treated with pindolol, a beta-adrenergic blocking drug with intrinsic sympathomimetic activity. To evaluate the interactions between beta-blockade, intrinsic sympathomimetic activity, and the level of pretreatment sympathetic activity, blood pressure, heart rate, and forced expiratory volume in one second (FEV1) were examined before and during a 15-week treatment program. The response of patients with a relatively higher pretreatment sympathetic tone reflected by a resting heart rate equal to or greater than 80 beats per minute (Group I) was compared with the response of patients with a lower pretreatment heart rate (less than 80 beats per minute) (Group II). Decreases in mean blood pressure were similar in the two groups. In patients in Group I, the net effect of pindolol was a modest decrease in heart rate and FEV1, supporting the concept that when sympathetic tone is relatively high, the beta-blocking effect is dominant. In contrast, patients in Group II showed little change in heart rate or FEV1 during pindolol treatment, reflecting a balance between the intrinsic sympathomimetic activity and beta-blocking effects of pindolol. Thus, the intrinsic sympathomimetic activity of pindolol is physiologically evident, and relative impact is dependent on the pretreatment level of sympathetic tone.

Clinical Trials as Topic↗
PubMed1983

Routine serum enzyme tests in the diagnosis of acute myocardial infarction. Cost-effectiveness.

To determine the cost-effectiveness of routine use of serial SGOT, lactic dehydrogenase (LDH), and LDH isoenzyme determinations in patients with suspected acute myocardial infarction (AMI), 166 consecutive patients admitted to a coronary care unit were prospectively identified and clinical findings analyzed independently using predetermined criteria. Based on chest pain characteristics, ECG, and creatine kinase--MB (CK-MB) results, patients were placed in categories of definite AMI (31%), possible AMI (34%), or AMI excluded (36%). The SGOT and/or LDH patterns were considered positive (ie, suggestive of AMI) in 82% of the patients with definite AMI but only confirmed CK-MB results. Positive SGOT/LDH results yielded new clinically relevant information in only 14 patients (8%). Total charges for SGOT/LDH determinations in these 166 patients totaled $10,938 or approximately $780 for each additional clinically important positive result. When serial ECG and CK-MB results are available, routine serial SGOT/LDH determinations are not justified.

Adult↗
PubMed1982

Pindolol and systolic time intervals in patients with hypertension.

Two studies of systolic time intervals (STIs) in patients with mild to moderate hypertension (HBP) revealed that no mean change in systolic intervals occurred with pindolol therapy, although some patients had significant alterations in their STIs. Pindolol responders with normal pretreatment preejection period to left ventricular ejection time (PEP/LVET) ratios had a significant increase in this ratio following pindolol therapy, whereas those with abnormal pretreatment PEP/LVET ratios had improvement in this ratio on administration of the drug. Patients on propranolol showed no change in PEP/LVET ratio. Propranolol administration slowed heart rate and lengthened Q-S2, S1-S2, and LVET, however, without altering the Q-S2 and LVET index, indicating that the changes were caused by the effect of propranolol on the heart rate alone. Chlorthalidone in high doses significantly reduced the Q-S2 index and the S1-S2 index, indicating that these changes were not caused by alteration of the heart rate. The second study suggests that STIs may provide a predictive clue for clinical response to pindolol. Patients with normal cardiac function (group I) are more likely to respond to pindolol than are those with abnormal cardiac function (group II). Directionally opposite changes in STIs in the two subgroups suggest different mechanisms for changing cardiac function. Pindolol's dual role as a beta-blocking agent with intrinsic sympathomimetic activity is proposed as a possible explanation, beta-blocking effects predominating in group I and sympathomimetic activity balancing the beta effect in group II.

Adult↗
PubMed1982

Acute cardiogenic pulmonary edema in the elderly: factors predicting in-hospital and one-year mortality.

This prospective evaluation of 55 consecutive patients, aged 60 years or older, admitted in 1977-1978 to a community hospital coronary care unit for treatment of cardiogenic pulmonary edema, examines morality during hospitalization and during the subsequent one-year follow-up. Their treatment was based on clinical criteria, without the "advantage" of Swan-Ganz catheters and before widespread use of vasodilators for severe congestive heart failure. Multiple clinical and laboratory features were reviewed to determine possible prognostic clues. The nine patients who died during the initial hospitalization provided several clues to immediate mortality, including admission systolic blood pressure of less than 150 mm Hg, dyspnea for more than four hours, and peak creatine kinase values greater than 1,000 IU/L. The study identified high-risk patients who may benefit from more aggressive in-hospital therapy. The one-year mortality among the 46 patients discharged from the hospital was high (43%). Most noninvasive methods were not useful in attempting to predict one-year survival. The important question of whether newer therapeutic methods including vasodilators will favorably alter the relatively poor long-term prognosis in the elderly needs further study.

Aged↗
PubMed1982

Collateral circulation in patients with unstable angina.

Coronary collaterals were evaluated in 218 consecutive catheterized patients with unstable angina (defined as ischemic cardiac pain at rest associated with transient electrocardiographic changes). Collaterals were present in 106 patients (49 percent). The presence of collaterals correlated with the extent and severity of the coronary artery disease but not with age, sex, or risk factors. Among patients with comparable severity of narrowings, the presence of collaterals did not appear to protect against abnormal wall motion or pathologic Q waves on the ECG. In patients with single vessel disease, collaterals also did not appear to protect against transient ST segment evaluation during ischemia.

Age Factors↗
PubMed1980

Relation of ventricular premature beat suppression to serum quinidine concentraton determined by a new and specific assay.

Fourteen patients who were receiving quinidine in doses of 800 to 1800 mg. per day for ventricular arrhythmias underwent Holter monitoring during a steady state dosing interval at a mean of four days after the initiation of quinidine therapy. Serum quinidine concentration, determined by a specific high performance liquid chromatography method, was measured hourly during the dosing interval. Ventricular premature beat (VPB) frequency during quinidine therapy was compared to the baseline VPB frequency. A reduction in VPB frequency of at least 90% was required to substantiate the presence of a therapeutic response to quinidine. In 12 of the 14 patients a therapeutic response to quinidine was present at serum levels ranging from 0.72 to 5.92 micrograms/ml. There was no group correlation between serum quinidine concentration and VPB frequency, but there was a tendency in individual patients for VPB frequency to decrease as serum quinidine level increased. Quinidine toxicity was not observed in these 14 patients. Because of the wide variation in response to quinidine, a serum quinidine concentration that is within the therapeutic range is not necessarily the optimal serum quinidine concentration for an individual patient. The clinician may therefore consider increasing the dose if there is no evidence of quinidine toxicity and the ventricular rhythm disturbance is not adequately controlled.

Aged↗
PubMed1980

ECG predictors of coronary anatomy and left ventricular function. Findings in patients with typical angina pectoris.

In 90 patients with typical angina pectoris, resting ECGs and cardiac catheterization findings were independently reviewed to determine whether ECG findings could be used to predict the extent of disease and the state of the left ventricular (LV) function. Thirty consecutive patients in each of three ECG groups were studied: group 1, normal ECG: group 2, ST-T abnormalities; and group 3, Q wave infarction pattern. Triple vessel disease was present in 30 percent, 40 percent, and 66 percent of patients in groups 1, 2, and 3, respectively. The ejection fraction (percent) (mean +/- SD) was 65 +/- 12, 64 +/- 11, and 51 +/- 16 in groups 1, 2, and 3, respectively. With increasing ECG abnormality (group 1 to group 3), there was a tendency to both more extensive coronary disease and greater depression of left ventricular function. However, the resting ECG appeared to correlate bettter with the state of the LV function than with the extent of the coronary artery disease.

Angina Pectoris↗
PubMed1980

Systemic sarcoidosis and electrocardiographic conduction abnormalities. Electrophysiologic evaluation of two patients.

Two patients with long histories of sarcoidosis had progression of conduction abnormalities to heart block and severe bradycardia. Conduction system involvement was trifascicular in both patients, though evidence for left ventricular functional impairment was otherwise lacking. Sudden death is seen more commonly in patients with sarcoidosis who have diffuse myocardial involvement, while conduction abnormalities can occur with relatively localized disease.

Arrhythmias, Cardiac↗
PubMed1979

Quinidine therapy in hospitalized patients with ventricular arrhythmias.

Quinidine serum levels and pharmacokinetic data were assessed during steady state therapy with oral quinidine sulfate in 19 hospitalized patients who were being treated for ventricular arrhythmias. A new high performance liquid chromatography assay was employed. Four patients were studied both after the first dose of quinidine and at steady state, and the initial dose pharmacokinetic values were found not to be predictive of steady state. The mean half-life of quinidine was 4.5 hours, but there was wide individual variation. The elimination rate constant for quinidine was significantly lower in patients with echocardiographic evidence of left ventricular dilatation than in patients with normal echocardiographic left ventricular size. The average urinary excretion of quinidine was only 11.3%. The pharmacokinetic data in seven chronic alcoholic patients without clinical or laboratory evidence of hepatic insufficiency did not differ from the data obtained in nonalcoholic patients. However, with severely impaired liver function, there may be marked prolongation of quinidine half-life predisposing to quinidine toxicity. The possible clinical implications of these findings are discussed.

Aged↗
PubMed1979

Transient S-T segment elevation in unstable angina: prognostic significance.

The clinical and prognostic significance of the direction of the S-T segment shift on the 12-lead electrocardiogram was evaluated in medically treated patients with unstable angina pectoris. Long-term mortality and morbidity of 11 patients with transient S-T segment elevation (group I) were compared to that of 21 patients with transient S-T segment depression (group II). The average follow-up duration was 62 months. There was no significant difference between groups I and II with respect to survival or nonfatal myocardial infarction over a five-year period. Mortality was related to the extent of coronary artery disease and left venticular ejection fraction rather than to the direction of the S-T segment shift.

Adult↗
PubMed1979

Clinical indicators of left main coronary artery disease in unstable angina.

Two hundred consecutive catheterized patients with unstable angina pectoris were reviewed to find clinical and noninvasive indicators of left main coronary artery disease (greater than or equal to 50% lesion). Thirty-five patients (17.5% of total) had left main coronary artery disease. There were no differences between patients with and without left main coronary artery disease in age, sex, results of resting electrocardiogram, congestive heart failure, dyspnea during pain, duration of longest pain, arrhythmias, response to medical therapy, or other risk factors. Crescendo angina pectoris (worsening of pre-existing angina), transient ST-segment depression with pain, simultaneous anterior and inferior ST changes during pain, and fluoroscopic calcification of the left main coronary artery were all significantly more common in patients with left main coronary artery disease. However, low sensitivity or low predictive value, or both, limit the usefulness of these clinical predictors. Left main coronary artery disease cannot be reliably predicted in patients with unstable angina pectoris before coronary arteriography.

Angina Pectoris↗