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Biomedical subjects

J M Nicklas

Publications and source records attributed to J M Nicklas.

At least 19 recordsLinked to original sources
PubMed1991

Prospective, double-blind, placebo-controlled trial of low-dose amiodarone in patients with severe heart failure and asymptomatic frequent ventricular ectopy.

Sudden cardiac death is a common cause of mortality in patients with congestive heart failure. To determine if low-dose amiodarone could reduce sudden death among these patients, a prospective, placebo-controlled, double-blind pilot trial was conducted. One hundred one patients with ejection fractions less than 30%, New York Heart Association class III or IV symptoms, and frequent but asymptomatic spontaneous ventricular ectopy (Lown class II to V) were randomly assigned to treatment with low-dose amiodarone (400 mg/day for 4 weeks and then 200 mg/day) or placebo. Mean follow-up was 357 days (range 4 to 1009 days). Side effects were infrequent and there was no difference in the incidence of side effects between the treatment groups. The frequency of spontaneous ventricular ectopy in the group receiving amiodarone fell from 4992 +/- 1240 beats/24 hours at baseline to 1135 +/- 494 beats/24 hours after 1 month of treatment (p = 0.02) and remained low after 6 months, while there was no change in ventricular ectopy among the patients receiving placebo. Despite the reduction in ectopy, there was no improvement in mortality or decrease in the incidence of sudden death. One-year mortality by Kaplan-Meier analysis was 28% in the group receiving amiodarone and 19% in the group receiving placebo (p = NS). One-year mortality in patients with greater than 75% reduction in ventricular ectopy after 1 month of treatment was 31% versus 17% in patients with less than or equal to 75% ectopic suppression (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Treatment of cardiogenic shock with the Hemopump left ventricular assist device.

A multiinstitutional study is in progress to evaluate the Hemopump in the treatment of cardiogenic shock. Fifty-three patients with refractory cardiogenic shock were selected for Hemopump assistance. The hemodynamic definition of cardiogenic shock included (1) a cardiac index of less than 2.0 L.min-1.m-2, (2) pulmonary capillary wedge pressure of greater than 18 mm Hg, and (3) a systolic blood pressure of less than 90 mm Hg or a left ventricular work index of less than 1,500 g-m.m-2.min-1. The Hemopump was successfully inserted in 41 of 53 patients (77.3%). A significant improvement in the hemodynamic status was seen during Hemopump assistance. A minimal level of hemolysis was observed. No leg ischemia was observed. The 30-day overall survival of the Hemopump group was 31.7%. Criteria establishing indications for use and clinical utility are proposed. We conclude that the Hemopump provides significant hemodynamic support of the patient in cardiogenic shock allowing for recovery from ventricular stunning in marginal ventricles, and that in select patients the Hemopump may offer a major improvement in survival over conventional therapy.

Cardiac Output↗
PubMed1991

Computer analysis of physiologic signals in a cardiovascular research laboratory.

A comprehensive computer program which provides immediate computation and feedback has been developed for data acquisition and analysis of signals in a cardiovascular animal laboratory. The system is based on a microcomputer equipped with analog-to-digital converter and supports function modules which digitize, filter, and differentiate up to 8 simultaneously sampled cardiovascular signals. The program detects, analyses, and plots incoming and averaged beats. Beat-by-beat signal averaging for each channel is performed and cardiac cycles are partitioned automatically. For each cardiac and average cycle the amplitude at 6 physiologic fiducial markers are measured and derived calculations are made. Channel vs channel plots and loop area measurements are also computed and displayed. The computer algorithms have been shown to give accurate, precise, and reproducible results when tested on canine cardiovascular data. Also, it has been demonstrated that signal averaging is an appropriate analysis technique for cardiovascular signals.

Algorithms↗
PubMed1989

Natriuresis associated with elevated plasma atrial natriuretic hormone during supraventricular tachycardia.

Elevated plasma levels of atrial natriuretic hormone (ANH) have been found in patients during paroxysmal supraventricular tachycardia (SVT) and other clinical syndromes. However, physiologic effects of this endogenous ANH have not been demonstrated. To determine whether the rise in ANH during SVT is associated with either a natriuresis or kaliuresis, urine sodium and potassium levels were measured in five patients at baseline and during SVT simulated by rapid atrioventricular pacing. Plasma ANH levels increased from 149 +/- 35 pmol/L at baseline to 187 +/- 31 pmol/L (p = 0.007) during SVT. Plasma vasopressin and renin levels were unchanged. Urine sodium levels increased 49% from 1.54 +/- 0.66 mEq/hr at baseline to 2.29 +/- 0.89 mEq/hr (p = 0.044) during SVT, and urine potassium levels increased 22% from 4.14 +/- 0.10 mEq/hr to 5.04 +/- 1.25 mEq/hr (p = 0.018). Urine sodium and potassium levels returned to baseline values 1 hour after pacing. Thus elevated plasma levels of ANH during SVT are associated with both a natriuresis and kaliuresis, which may represent physiologic effects of the endogenously secreted hormone.

Atrial Natriuretic Factor↗
PubMed1989

Amrinone versus conventional therapy in pulmonary hypertensive patients awaiting cardiac transplantation.

Pulmonary hypertension is associated with an increased perioperative mortality for orthotopic heart transplantation. A transpulmonary gradient greater than 15 mm Hg or a pulmonary vascular resistance greater than 5 Woods units increases mortality secondary to right heart failure. This study compares amrinone with conventional therapy in 38 transplant candidates with pulmonary hypertension. All patients had elevated transpulmonary gradient, pulmonary vascular resistance, or both. Group 1 (n = 21) received prolonged continuous intravenous amrinone therapy, whereas group 2 (n = 16) received high-dose oral diuretics, digitalis, and captopril. Both groups 1 and 2 had decreased pulmonary hypertension, transpulmonary gradient, and pulmonary vascular resistance. However, amrinone was more effective, with a 86% response rate versus 63% response for conventional therapy. Survival awaiting transplantation was significantly higher in group 1 (20 of 22, 91%) than in group 2 (10 of 16, 63%). Although both groups 1 and 2 had significantly decreased pulmonary vascular resistance, only group 2 had significantly decreased systemic vascular resistance. Comparison of pulmonary vascular resistance after therapy showed that the response in group 1 (amrinone) was significantly lower than the response in group 2 (conventional therapy), suggesting that amrinone may function as a direct vasodilator of the pulmonary vasculature. There were no operative deaths or episodes of perioperative right heart failure in either group. Amrinone appears to be more effective and safe than conventional therapy in the treatment of prospective heart transplant candidates with pulmonary hypertension.

Adult↗
PubMed1989

An algorithm for the quantification of ST-T segment variability.

A template boundary algorithm which quantitatively determines repolarization (ST-T segment) variability in a normal population has been developed. The algorithm defines an initial ST-T template for comparison with successive beats. Variability is quantified using boundary limits around the template which are widened, when necessary, to included incoming ST-T segments. The boundaries at the end of each hour are stored and the collection of boundaries over a set of normal subjects quantifies the normal variation over the entire ST-T segment. The algorithm can be used to determine prospectively normal ST-T variability based on a regression analysis of R-wave or T-wave amplitude, and QT interval. Application of these boundary predictions should be useful in distinguishing repolarization changes secondary to ischemia from normal variability.

Algorithms↗
PubMed1989

Randomized, double-blind, placebo-controlled trial of tissue plasminogen activator in unstable angina.

Angiographic, angioscopic and pathologic reports have recently demonstrated a high incidence of intracoronary thrombus in patients with unstable angina. To determine if thrombolysis could be beneficial when combined with maximal medical therapy, 40 patients with rest angina, angiographically documented coronary artery disease and pacing-induced ischemia were randomly assigned to intravenous recombinant tissue-type plasminogen activator (rt-PA, 150 mg/8 h) or placebo in a prospective double-blind trial. All patients received nitrates, a beta-adrenergic blocking agent, a calcium channel blocker, aspirin and heparin. Pacing thresholds for ischemia and quantitative coronary stenosis were measured before and after infusion of the study medication. Intracoronary thrombus was identified angiographically before infusion of the study medication in 16 patients; 7 received rt-PA and 9 received placebo. The ischemic pacing threshold in patients treated with rt-PA increased from 112 +/- 4 beats/min at baseline to 127 +/- 5 beats/min (p = 0.007) by the end of the infusion versus an insignificant change in patients who received placebo (from 116 +/- 4 to 119 +/- 4 beats/min, p = NS). In patients with intracoronary thrombus, the ischemic pacing threshold increased 26 +/- 7 beats/min with rt-PA treatment versus 0 +/- 3 beats/min with placebo (p = 0.004). In contrast, in patients without thrombus, there was no difference in ischemic pacing threshold increments between treatment groups (7 +/- 11 beats/min for rt-PA versus 6 +/- 5 beats/min for placebo, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Decreased coronary flow reserve after transient myocardial ischemia in dogs.

The effect of a transient (15 min) period of regional ischemia on coronary flow reserve in the postischemic myocardium was studied in 24 open chest dogs. Coronary flow was measured with electromagnetic flow probes, and flow reserve was determined during reactive hyperemia after 30 s coronary occlusions and during intracoronary infusions of adenosine. Measures of flow reserve after 15 min of ischemia were made after coronary flow returned to basal levels and flow reserve was then monitored for 1 h. All measures of coronary flow reserve were significantly reduced after transient ischemia: peak flows during reactive hyperemia and intracoronary adenosine infusions decreased by 20 and 24%, respectively, the peak/basal flow ratio by 16% and the repayment/debt ratio by 54%; minimal coronary vascular resistance during reactive hyperemia and intracoronary adenosine increased by 29 and 33%, respectively. Abnormal flow reserve was present for at least 1 h. No changes in flow reserve were detected in control animals over the same time period. Thus, a transient period of myocardial ischemia significantly decreases coronary flow reserve for a prolonged period of time. This "vascular stunning" must be considered when flow reserve is used to assess the functional significance of a coronary stenosis and could be the cause of variable exercise tolerance in patients with angina pectoris.

Animals↗
PubMed1988

Coronary revascularization after intravenous tissue plasminogen activator for unstable angina pectoris: results of a randomized, double-blind, placebo-controlled trial.

To determine the role of intravenous tissue plasminogen activator (t-PA) in unstable angina, it was compared with placebo in a randomized, double-blind trial. Forty patients with angina at rest and provocable ischemia (pacing induced) had baseline coronary angiography, study drug infusion and then repeat angiography at 20 +/- 9 hours. All patients received diltiazem, nitrates, beta blockers, aspirin and intravenous heparin. During study drug infusion (150 mg over 8 hours), refractory ischemia necessitating emergency bypass surgery (CABG) or coronary angioplasty (PTCA) occurred in 4 of 20 t-PA patients compared with 1 of 20 placebo patients (p = 0.21). Before discharge, revascularization for persistent, provocable ischemia and a residual stenosis greater than or equal to 60% was as follows: t-PA patients, 8 PTCA and 7 CABG; placebo patients, 11 PTCA and 8 CABG (p = 0.39). Quantitative angiographic percent diameter stenosis of the culprit artery at baseline and follow-up was: t-PA 71 +/- 17 and 63 +/- 22; placebo 70 +/- 19 and 67 +/- 22 (difference not significant). However, 3 t-PA patients compared with no placebo patients demonstrated an insignificant (less than 60% diameter) residual stenosis and averted PTCA (p = 0.14). There were no complications of PTCA in the 8 t-PA patients; in contrast, 3 of 11 placebo patients had abrupt closure, necessitating emergency CABG in 2 (p = 0.23). Thus, intravenous t-PA in unstable angina can eliminate the need for PTCA in a few patients, does not appear to decrease the overall or emergency rate of revascularization procedures and may facilitate the safety of PTCA.

Angina Pectoris↗
PubMed1988

Kinetics, dynamics, and bioavailability of bumetanide in healthy subjects and patients with congestive heart failure.

Four healthy subjects and six patients with congestive heart failure (CHF) were given 3 mg oral and intravenous doses of bumetanide in a random crossover fashion. Bumetanide was analyzed by HPLC, and sodium and potassium was analyzed by flame photometry. Aside from a modest reduction in renal clearance, the kinetics of bumetanide in CHF were similar to those in healthy subjects. The extent of bioavailability was 81%, with a variability of 20% to 25% about the mean for both groups. The cumulative dynamic responses to bumetanide, whether administered orally or intravenously, were essentially the same in each group. Pharmacodynamic modeling showed that there were no significant differences between healthy subjects and patients with CHF in either ER50 (bumetanide urinary excretion rate producing 50% of maximum drug effect) or S (slope), although the baseline effect was 15 times lower in CHF. The maximum effect attributable to bumetanide was twofold higher in healthy subjects and there was a significant correlation between this parameter and creatinine clearance (r = 0.964; p less than 0.001). Overall, these results indicate that a predictable transition from 3 mg intravenous to oral doses of bumetanide is possible in CHF.

Administration, Oral↗
PubMed1987

Exercise testing three days after onset of acute myocardial infarction.

To determine the feasibility and predictive value of early exercise testing 72 hours after acute myocardial infarction, 109 consecutive patients who received reperfusion therapy were prospectively evaluated. In the group studied, in 87 (80%) the course was uncomplicated 3 days after admission, as defined by a lack of congestive heart failure, arrhythmias and angina, and 53 patients (49%) performed heart rate-limited (140 beats/min) treadmill exercise. These patients exercised for 7.9 +/- 3.4 minutes, achieving a heart rate of 129 +/- 11 beats/min and a systolic blood pressure of 151 +/- 27 mm Hg. The exercise test was not accompanied by any protracted ischemia, infarction or significant arrhythmias. Accompanying tomographic thallium-201 scintigraphy demonstrated a reversible perfusion defect in 14 patients (26%), no evidence for ischemia in 36 patients (69%) and an equivocal result in 3 patients (6%). Of the 14 patients with a positive exercise-thallium test result, 4 had an adverse clinical outcome of either reinfarction, postinfarction angina or ventricular tachycardia during hospital days 4 to 10; an adverse in-hospital outcome was not seen in the 40 patients with a negative exercise-thallium test result (p = 0.009). Thus, early exercise testing after acute myocardial infarction is safe in selected patients with an uncomplicated course and the test is predictive of in-hospital clinical outcomes.

Adult↗
PubMed1987

Quantitative measurement of coronary flow during medical revascularization (thrombolysis or angioplasty) in patients with acute infarction.

This study quantitatively evaluated the change in myocardial blood flow resulting from medical revascularization in patients with acute anterior myocardial infarction. Changes in great cardiac vein flow were measured using a thermodilution technique in 13 patients with acute infarction; 3 received intracoronary streptokinase and 10 percutaneous transluminal angioplasty. Average great cardiac vein flow during left anterior descending coronary artery occlusion was 62 +/- 6 ml/min and increased to 70 +/- 7 ml/min (p = 0.039) after arterial recanalization. There was significant individual variability in the great cardiac vein flow increments that was highly predictive of functional recovery as expressed by the change in ejection fraction at 7 to 10 days (r = 0.93, p = 0.0008). Incremental great cardiac vein flow was inversely correlated with the degree of residual stenosis and the duration of ischemia (r = 0.88, p = 0.0007). Patients with residual stenosis less than or equal to 50% had a significantly larger increase in great cardiac vein flow (14 +/- 5 ml/min) than did those with residual stenosis greater than 50% (0 +/- 2 ml/min, p = 0.026). Neither preinterventional left ventricular ejection fraction, hemodynamics nor age predicted incremental great cardiac vein flow. Therefore, quantitative measurements of great cardiac vein flow during medical revascularization in patients with an acute anterior myocardial infarction demonstrate variable reflow that is physiologically significant. A high grade residual stenosis and prolonged period of ischemia limit large increases in flow and prevent functional recovery. This study emphasizes the fact that recanalization in itself cannot be used as an indicator of the success of interventions designed to produce myocardial reperfusion.

Acute Disease↗
PubMed1987

Development of a template boundary algorithm to determine the ST-T threshold for silent ischemia.

A template boundary algorithm which quantitatively determines ST-T variability has been implemented and tested using seven normal patients. Relatively uniform variability was demonstrated throughout the ST-T segment in these patients during single lead continuous electrocardiographic monitoring at bedrest. The range of variability appears to be a function of both R wave and T wave amplitude. This algorithm appears to have potential utility in defining the ischemic criteria for silent ischemia.

Algorithms↗