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Biomedical subjects

C R Lambert

Publications and source records attributed to C R Lambert.

At least 73 records · Page 4Linked to original sources
PubMed1987

Effects of nicardipine on exercise- and pacing-induced myocardial ischemia in angina pectoris.

To define the effects of nicardipine, a new dihydropyridine calcium antagonist drug, on exercise- and pacing-induced myocardial ischemia, 15 men with coronary artery disease were studied during cardiac catheterization. Nicardipine was administered intravenously as a 2-mg bolus followed by an infusion titrated to maintain a 10- to 20-mm Hg decrease in systolic arterial pressure. At rest, nicardipine decreased systemic and coronary vascular resistances, left ventricular end-diastolic pressure and increased coronary blood flow, heart rate and myocardial oxygen consumption. During bicycle exercise-induced myocardial ischemia, nicardipine significantly prolonged exercise duration and time to 1 mm of ST-segment depression. These changes were associated with no alteration in the product of systolic pressure and heart rate, decreased left ventricular end-diastolic pressure, systemic and coronary vascular resistances and increased coronary blood flow, as well as myocardial oxygen consumption. During atrial pacing, the heart rate threshold for myocardial ischemia was not changed by nicardipine administration, despite improvement in the ratio of coronary blood flow to myocardial oxygen consumption and hemodynamic changes otherwise similar to those during exercise. Nicardipine favorably influenced myocardial metabolic state, as indexed by lactate extraction during pacing-induced ischemia. Nicardipine is a potent coronary and systemic vasodilating drug that improves exercise tolerance and myocardial metabolic response to pacing stress, the mechanism for which appears to be partially mediated through increased coronary blood flow.

Angina Pectoris↗
PubMed1987

Effects of titrated beta blockade (metoprolol) on silent myocardial ischemia in ambulatory patients with coronary artery disease.

This study investigates effects of beta-adrenergic blockade on total silent ischemic time assessed by ambulatory electrocardiographic monitoring and its relation to heart rate and time of day in ambulatory men with coronary artery disease. Metoprolol, when titrated to optimal dose in a controlled trial in 9 patients, reduced both total silent ischemic time (from 156 +/- 65 to 20 +/- 15 minutes, p = 0.04) and frequency of silent ischemic episodes (from 8 +/- 2 to 2 +/- 2 episodes, p = 0.03) compared with placebo. Mean daily heart rate was reduced, from 82 +/- 2 beats/min during placebo to 58 +/- 1 beats/min, as was heart rate at onset of 1 mm of ST-segment depression (106 +/- 2 to 74 +/- 4 beats/min, both p less than 0.001). Heart rate increased 10 +/- 1 beats/min during silent ischemia with placebo therapy, but increased only 4 +/- 1 beats/min during metoprolol treatment (p less than 0.03). During placebo administration the largest proportion of silent ischemic time occurred between 0600 and 1200 hours. Metoprolol attenuated this circadian variation in silent ischemia while reducing (p less than 0.05) total silent ischemic time in all periods. Thus, beta-adrenergic blockade reduces the frequency of silent myocardial ischemic episodes and total silent ischemic time, while mean daily heart rate and heart rate at onset of ischemia and maximal ischemia decrease. Metoprolol treatment also attenuates circadian variation of silent ischemia. These data may be interpreted to suggest that beta-adrenergic activation operates in the pathogenesis of silent myocardial ischemia and its circadian variation.

Aged↗
PubMed1987

Usefulness of nicardipine for angina pectoris.

Nicardipine treatment has been evaluated in patients with chronic stable effort angina or with angina at rest due to coronary spasm. Acute studies in patients with effort angina suggest a very favorable hemodynamic profile characterized by coronary vasodilatation and reduction in determinants of myocardial oxygen demand. Both open and controlled trials in patients with effort angina show that long-term oral administration increases exercise time and time to onset of 1 mm ST-segment depression and decreases angina frequency. With treatment for up to 6 months, antiischemic effects were maintained without serious adverse reactions. Other studies indicate that nicardipine is generally comparable to propranolol and nifedipine in prolonging exercise time and time to onset of ST-segment depression. Nicardipine, however, does not depress heart rate at rest, and maximal exercise workload is higher with nicardipine than with either placebo or propranolol. In a controlled study of patients with angina at rest due to coronary spasm, nicardipine decreased angina frequency and nitroglycerin consumption by approximately 80%. Episodes of symptomatic and asymptomatic ST-segment shift, as recorded by ambulatory electrocardiographic monitoring, showed a trend to decrease in number. Nicardipine appeared similarly effective in patients with coronary spasm superimposed on significant coronary disease and with spasm in the absence of significant coronary disease. Nicardipine appears to be safe and effective in the management of patients with angina pectoris.

Angina Pectoris↗
PubMed1987

Silent myocardial ischemia during daily activities in asymptomatic men with positive exercise test responses.

The usefulness of prolonged ambulatory electrocardiographic monitoring (AEM) for detecting ischemia was investigated in 17 asymptomatic men who had ischemic-type ST-segment depression (greater than or equal to 2.0 mm) during treadmill exercise testing. No patient took anti-ischemic medications and all patients underwent coronary angiography. A total of 1,154 hours (range 64 to 72 hours/patient) of high-quality AEM recordings was obtained. Silent ischemia (episodes of asymptomatic ischemic-type ST depression of 60 seconds or longer) occurred in 11 patients during daily activity detected by AEM. In 6 other patients, no myocardial ischemic episodes were found. But 1 of these patients withdrew after only 24 hours of AEM and the remaining 5 had no significant coronary artery disease (CAD). All 11 patients who had silent ischemia had significant CAD (at least 50% stenosis) on angiography. There was wide intrapatient variability in the frequency of silent ischemic episodes. Silent ischemia was identified in 6 of these 11 patients after 24 hours of AEM, in 2 after 48 hours and in 3 after 72 hours. Thus, asymptomatic men with positive exercise test responses and CAD have silent ischemic episodes during daily activity. AEM may be useful in helping to predict which patients with asymptomatic positive exercise test responses have CAD; however, extended AEM periods are required.

Activities of Daily Living↗
PubMed1986

Left ventricular dyskinesia reversed by intravenous nitroglycerin: a manifestation of silent myocardial ischemia.

Patients with coronary artery disease (CAD) frequently have left ventricular (LV) wall motion abnormalities in the absence of symptoms. Thirty-one patients with such LV wall motion abnormalities in the absence of symptoms participated in a study of the response of these abnormalities to ascending doses of intravenous nitroglycerin (NTG). In a subgroup of 20 patients the relation between the location of LV wall motion abnormalities and the presence or absence of significant CAD (greater than or equal to 50% diameter reduction), in the vessel supplying the LV region, was assessed. Wall motion improved after intravenous NTG; the ejection fraction increased by 3.7% (mean p less than 0.05) and by 9.4% in the 19 patients who responded. There was no significant increase in heart rate; both LV systolic and end-diastolic pressures decreased minimally (12.5 and 3.5 mm Hg, respectively, p less than 0.05). The ejection fraction response was observed with NTG doses less than or equal to 200 micrograms and no dose-response relation was apparent. In the subgroup subjected to regional wall motion analysis, the presence of dyskinesia was significantly (p = 0.007) associated with the presence of important CAD in a vessel supplying that region. Further, the fact that wall motion improvement after NTG was significantly (p = 0.002) associated supports the concept that silent ischemia results in LV regional wall motion abnormalities, which can be reversed with low dose intravenous NTG.

Adult↗
PubMed1986

Low-frequency requirements for recording ischemic ST-segment abnormalities in coronary artery disease.

The objective of this investigation was to determine whether extended low-frequency response is required to record ischemic ST-segment abnormalities in humans. Bipolar electrocardiograms (ECGs) were recorded in 5 men with coronary artery disease using a high-fidelity instrumentation amplifier and FM tape recorder before, during and after erect bicycle exercise. In all patients, ischemic ST-segment abnormalities developed during exercise; 3 patients had angina and 2 remained asymptomatic throughout the test. Using a fast-Fourier transform (FFT) and a variable digitizing rate into a 1,024-point input array, FFT spectra were computed with low-frequency content extending to either 0.20, 0.98 or 1.95 Hz for both a rest and exercise ECG. From these spectra, ECGs were resynthesized using the inverse FFT and compared with the original records. Visual inspection of the original and resynthesized ECGs revealed no obvious differences when low-frequency content extended to 0.20, 0.98 or 1.95 Hz. Numerical comparisons were made by calculating the coefficient of determination (R2) between the original and resynthesized ECGs. The R2 (mean +/- standard deviation) for these comparisons was 0.998 +/- 0.001. It is concluded that the amplitude-response characteristics of electrocardiographic recording equipment do not require extended low-frequency range (such as that found in FM systems) to accurately reproduce ischemic ST-segment abnormalities in humans.

Coronary Disease↗
PubMed1986

Effects of nicardipine on left ventricular function and energetics in man.

The effects of nicardipine, a new dihydropyridine calcium antagonist, on left ventricular function and energetics were studied in 13 patients. Nicardipine was administered as a 2 mg bolus (i.v.) followed by an infusion titrated to maintain a 10-20 mm Hg decrease in systolic pressure. Nicardipine increased heart rate 19% (P less than 0.001) while left ventricular end-diastolic pressure was not significantly changed and stroke volume (ml) increased 13% (P less than 0.01). Peak values for the first and second time derivatives of left ventricular pressure were increased by 26% (P less than 0.01) and 50% (P less than 0.02) respectively. Peak aortic blood flow, peak aortic blood acceleration, and the peak rate of change of ejection power were increased 86% (P less than 0.001), 123% (P less than 0.01), and 113% (P less than 0.001), respectively. Stroke work was not changed during nicardipine infusion. External power increased by 40% (P less than 0.01); however, the ratio of oscillatory to total power was not significantly different. Although the product of heart rate and systolic aortic pressure was not significantly altered with nicardipine, myocardial oxygen consumption increased 18% (P less than 0.02) with a disproportionate increase in coronary blood flow of 41% (P less than 0.001) and decrease in coronary resistance of 39% (P less than 0.001). The time constant for left ventricular isovolumic relaxation decreased 22% (P less than 0.001) during nicardipine infusion while the minimum value of dP/dt was unchanged. Thus, when administered intravenously in man, nicardipine is a potent coronary and systemic vasodilator producing reflex tachycardia, increased indices of myocardial contractile state, and improved isovolumic relaxation with an associated increase in myocardial oxygen consumption.

Angina Pectoris↗
PubMed1986

Tetraethylammonium-induced phasic arterial constriction: temporal and spatial characteristics.

In vitro techniques were developed to characterize temporal, spatial, and mechanical characteristics of tetraethylammonium (TEA)-induced phasic contractile activity in pressurized perfused canine femoral artery segments. Power spectral analysis revealed TEA-induced phasic activity to be included in the bandwidth from 0.004 to 0.016 Hz. The level of intraluminal pressure did not influence frequency characteristics of this activity. Mean total tangential stress increased proportionately with intraluminal pressure, whereas both mean developed tangential stress and the strain index mean percent change of external diameter showed a plateau in the 80- to 120-mmHg pressure range. TEA-induced phasic activity propagated longitudinally in all arteries studied. The velocity of longitudinal propagation (V, cm/s) varied with intraluminal pressure in a nonlinear fashion with V = 0.79 +/- 0.05 at 40 mmHg, V = 0.72 +/- 0.05 at 80 mm Hg, and V = 0.85 +/- 0.05 at 120 mmHg. V was not affected by tetrodotoxin, and phasic activity was abolished by verapamil. Phasic activity showed a primary direction of propagation 81 +/- 7% of the time; however, this direction was variable in all arteries. Thus vascular smooth muscle activation by TEA, which has been proposed as a model for coronary artery spasm, produces propagated constrictor responses in the ultra-low-frequency band with pressure-sensitive velocity characteristics and mechanical properties that are optimized in the physiological pressure range.

Animals↗
PubMed1986

Left ventricular function abnormalities as a manifestation of silent myocardial ischemia.

A large body of evidence exists indicating that left ventricular dysfunction is a common occurrence in patients with severe coronary artery disease and represents silent or asymptomatic myocardial ischemia. Such dysfunction probably occurs early in the time course of every ischemic episode in patients with coronary artery disease whether symptoms are eventually manifested or not. The pathophysiology of silent versus symptomatic left ventricular dysfunction due to ischemia appears to be identical. Silent ischemia-related left ventricular dysfunction can be documented during spontaneous or stress-induced perturbations in the myocardial oxygen supply/demand ratio. It also may be detected by nitroglycerin-induced improvement in ventricular function or by salutary changes in wall motion following revascularization. Silent left ventricular dysfunction is a very early occurrence during ischemia and precedes electrocardiographic abnormalities. In this light, its existence should always be kept in mind when dealing with patients with ischemic heart disease. It can be hypothesized that because silent ischemia appears to be identical to ischemia with symptoms in a pathophysiologic sense, prognosis and treatment in both cases should be the same.

Coronary Disease↗
PubMed1986

Detection of silent myocardial ischemia in patients with angina using continuous electrocardiographic monitoring.

In patients with effort angina, ST-segment depression is a reliable indicator of transient myocardial ischemia. Ambulatory electrocardiographic monitoring can detect episodes of ST-segment depression with and without chest pain in patients with coronary heart disease. This test provides valuable information about the presence, frequency, magnitude, and duration of transient myocardial ischemia and associated trigger factors.

Ambulatory Care↗
PubMed1985

Coronary and systemic hemodynamic effects of nicardipine.

Systemic and coronary hemodynamic effects of a new dihydropyridine calcium antagonist, nicardipine, were studied in 15 patients. Nicardipine was administered as a 2-mg bolus intravenously followed by an infusion titrated to maintain a 10 to 20-mm Hg decrease in systolic pressure. Nicardipine increased both heart rate from 69 +/- 3 to 81 +/- 3 beats/min and cardiac output from 7.3 +/- 0.5 to 9.9 +/- 0.5 liters/min (both p less than 0.001) as systemic vascular resistance decreased from 1,183 +/- 70 to 733 +/- 33 dynes s cm-5 (p less than 0.001). Left ventricular end-diastolic pressure remained constant, at 14 +/- 1 vs 14 +/- 1 mm Hg as stroke volume increased from 108 +/- 6 to 123 +/- 6 ml/m2 (p less than 0.001). Coronary blood flow increased from 102 +/- 9 to 147 +/- 13 ml/min, while coronary resistance decreased from 1.17 +/- 0.1 to 0.7 +/- 0.1 mm Hg/ml/min (both p less than 0.001). Heart rate-systolic blood pressure product did not change (104 +/- 5 vs 106 +/- 5 beats/min mm Hg X 10(-2), difference not significant) with drug administration. At the same heart rate before and during nicardipine administration (using atrial pacing in 6 patients), significant augmentation of coronary flow was still observed. Thirteen of 14 patients showed a greater percent decrease in coronary resistance than systemic vascular resistance. Nicardipine differs from other calcium antagonists with respect to consistent augmentation of coronary blood flow. This effect appears to be the result, in part, of increased potency in the coronary bed compared with the systemic vascular bed.

Aged↗
PubMed1985

Effects of muscle contraction on pulsatile pressure-flow relations in femoral bed.

Femoral arterial pressure-flow relations and vascular impedance were studied during isometric contraction of the gastrocnemius-plantaris muscle group in anesthetized dogs. Contractions were synchronized with the electrocardiogram to occur in the first or second half of the cardiac cycle and included twitches as well as low-, intermediate-, and high-frequency tetanuses. The effects of fatigue and recovery were also documented. Marked changes in pressure and flow waveforms and corresponding femoral arterial input impedance spectra were seen for all contraction modes. Impedance moduli and estimated characteristic impedance were elevated regardless of contraction mode and were associated with fluctuations in impedance phase. All tetanuses placed in the first half of the cardiac cycle produced a striking and consistent reversal of impedance phase for the fundamental harmonic from negative to positive values which decreased with progressive fatigue. During recovery, impedance spectra were unchanged from control spectra. We have demonstrated marked alterations in pressure and flow waveforms and impedance spectral patterns during isometric contraction in the canine hindlimb. These changes may be explained by 1) markedly increased wave reflection as a result of muscle contraction and/or 2) the generation of a retrograde pulse by contracting muscle that fuses with the antegrade pulse of cardiac origin.

Animals↗