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Biomedical subjects

M B Leon

Publications and source records attributed to M B Leon.

340 records · Page 19Linked to original sources
PubMed1985

Combination therapy with calcium-channel blockers and beta blockers for chronic stable angina pectoris.

Combination therapy using calcium-channel blockers and beta blockers in patients with refractory chronic stable angina has gained much popularity, but remains highly controversial because of the potential for serious additive deleterious hemodynamic or electrophysiologic reactions. In studies involving patients with preserved left ventricular function receiving chronic oral beta blockers, short-term administration of intravenous verapamil has been shown to cause a further lowering in heart rate and blood pressure while prolonging atrioventricular node conduction; additive cardiodepressant effects were noted, including a tendency toward increased left and right heart filling pressures. Nifedipine, on the other hand, when added acutely to beta blockers, causes an increase in heart rate, a decrease in blood pressure and either no change or a slight improvement in most cardiac performance variables. Controlled, double-blind clinical trials have demonstrated that combinations of calcium-channel blockers and beta blockers result in augmented symptom benefit compared with either drug class alone. The predominant mechanism responsible for such improvement is increased lowering of myocardial oxygen demand by virtue of additive diminution in heart rate, blood pressure and, consequently, pressure-rate product both at rest and during exercise. Verapamil (and possibly diltiazem) plus beta blockers appears to have the greatest therapeutic efficacy but also the highest frequency of harmful adverse cardiac effects, whereas nifedipine plus beta blockers is generally safer but also less efficacious. Factors that should be carefully considered by clinicians contemplating combination therapy are the choice of calcium-channel blocker, the dose of calcium-channel blocker and beta blocker, the presence of antecedent left ventricular dysfunction or conduction system disease and the possibility of drug interactions. Concomitant calcium-channel blocker and beta-blocker therapy is an important contribution to the pharmacologic management of resistant patients who remain symptomatic during single drug treatment. However, the possibility of additive adverse cardiac effects mandates careful patient selection and close clinical monitoring.

Adrenergic beta-Antagonists↗
PubMed1985

Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve.

Thirty-three patients with chest pain despite angiographically normal coronary arteries underwent both coronary flow studies during pacing and resting and exercise gated blood pool scintigraphy. During atrial pacing after administration of ergonovine, those patients developing their typical chest pain demonstrated significantly lower great cardiac vein flow (97 +/- 31 vs 150 +/- 33 ml/min, p less than .001), higher coronary resistance (1.27 +/- 0.43 vs 0.77 +/- 0.18 mm Hg/ml/min, p less than .005), and less lactate consumption (30.5 +/- 22.0 vs 69.7 +/- 41.1 mM . ml/min, p less than .005) and a higher left ventricular end-diastolic pressure after pacing (20 +/- 4 vs 12 +/- 1, p less than .001) compared with those without pain and in the absence of significant luminal narrowing of the epicardial coronary arteries. The 26 patients with abnormal vasodilator reserve demonstrated reduced left ventricular ejection fraction during exercise (58 +/- 8%) compared with the seven patients with appropriate vasodilator reserve (66 +/- 4%, p less than .05) and with a group of 52 control patients of similar age and sex distribution and free of known heart disease (66 +/- 10%, p less than .001). In addition, 12 of the 26 patients with abnormal vasodilator reserve demonstrated exercise-induced regional wall motion abnormalities. Many of these patients also manifested impaired left ventricular diastolic filling at rest compared with the control subjects (peak filling rate 2.6 +/- 0.7 vs 3.2 +/- 0.7 end-diastolic volume/sec, p less than .005). Thus, patients with chest pain resulting from abnormal vasodilator reserve demonstrate abnormalities of left ventricular systolic and diastolic function suggestive of myocardial ischemia.

Adult↗
PubMed1985

Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures.

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1982

Effects of verapamil and propranolol on left ventricular systolic function and diastolic filling in patients with coronary artery disease: radionuclide angiographic studies at rest and during exercise.

To determine the effects of verapamil on left ventricular (LV) systolic function and diastolic filling in patients with coronary artery disease (CAD), we performed gated radionuclide angiography at rest and during exercise in 16 symptomatic patients before and during oral verapamil therapy (480 mg/day). Twelve patients were also studied during oral propranolol (160--320 mg/day). LV ejection fraction at rest was normal in 13 patients, but abnormal diastolic filling at rest, defined as peak filling rate (PFR) less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 180 msec, was present in 15. During verapamil, resting ejection fraction decreased (control 50 +/- 10% [+/- SD), verapamil 45 +/- 12%, p less than 0.005), but resting diastolic filling improved: PFR increased (control 1.9 +/- 0.6 EDV/sec, verapamil 2.3 +/- 0.9 ECV/sec, p less than 0.005) and time to PFR decreased (control 185 +/- 38 msec, verapamil 161 +/- 27 msec, p less than 0.05). Exercise ejection fraction did not change during verapamil (control 42 +/- 13%, verapamil 43 +/- 12%, NS), but exercise PFR increased (control 3.1 +/- 0.9 EDV/sec, verapamil 3.6 +/- 1.1 EDV/sec, p less than 0.05) and exercise time to PFR decreased (control 108 +/- 30 msec, verapamil 91 +/- 17 msec, p less than 0.05). In contrast, propranolol did not alter ejection fraction, PFR, or time to PFR at rest or during exercise. Thus, LV ejection fraction is decreased by verapamil at rest but is unchanged during exercise. While LV systolic function is not improved by verapamil, LV diastolic filling is enhanced by verapamil, both at rest and during exercise. These mechanisms may account in part for the symptomatic improvement in many patients during verapamil therapy.

Adult↗
PubMed1981

Impaired left ventricular diastolic filling in patients with coronary artery disease: assessment with radionuclide angiography.

To assess left ventricular (LV) diastolic filling at rest in patients with coronary artery disease (CAD), we analyzed high-resolution time-activity curves (10-20 msec/frame) obtained from gated radionuclide angiograms in 231 patients. Peak LV filling rate (PFR), expressed in end-diastolic volumes per second (EDV/sec), was subnormal in CAD patients (1.8 +/- 0.6 [+/- SD] vs normal mean of 3.3 +/- 0.6, p les than 0.001) and time to PFR (TPFR), measured from end-systole to PFR, was prolonged (171 +/- 41 msec vs normal mean of 136 +/- 23 msec, p less than 0.001). These indexes were also abnormal in the 141 patients with normal resting LV ejection fraction (PFR = 2.1 +/- 0.5 EDV/sec; TPFR = 175 +/- 36 msec) and in 123 patients without Q waves on the ECG (PFR = 2.1 +/- 0.5 EDV/sec; TPFR = 168 +/- 38 msec). Abnormal LV filling at rest (PFR less than 2.5 EDV/sec or TPFR greater than 180 msec) was found in 91% of all patients with CAD, 86% of patients with normal resting LV ejection fractions, 85% of patients without Q waves, and 82% of patients with normal resting LV ejection fraction, no resting regional wall motion abnormalities and no Q waves. Thus, LV diastolic filling, evaluated noninvasively by radionuclide angiography, is abnormal in a high percentage of patients with CAD at rest independent of LV systolic function or previous myocardial infarction.

Adult↗
PubMed1981

Effects of verapamil on left ventricular systolic function and diastolic filling in patients with hypertrophic cardiomyopathy.

Verapamil improves exercise capacity in patients with hypertrophic cardiomyopathy (HCM), but its mechanism of action are unknown. We examined the effects of oral verapamil (320-480 mg/day) on resting left ventricular (LV) systolic and diastolic function in patients with HCM. High-temporal-resolution time-activity curves from gated technetium-99m radionuclide angiograms were analyzed before and after verapamil therapy in 40 patients, of whom 16 were also studied during propranolol therapy (80-960 mg/day). All but one patient had normal or supranormal systolic function, but 70% had evidence of diastolic dysfunction, defined as peak LV filling rate (PFR) less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 80 msec. Verapamil did not change LV ejection fraction, peak ejection rate or ejection time, but did increase PFR (control 3.3 +/- 1.0 EDV/sec, verapamil 4.1 +/- 1.1 EDV/sec; p less than 0.001) and reduce time to PFR (control 187 +/- 56 msec, verapamil, 159 +/- 34 msec; p less than 0.001). Only 30% of patients had evidence of diastolic dysfunction during verapamil. In contrast, propranolol did not change LV ejection fraction, PFR or time to PFR, but did prolong ejection time and reduce peak ejection rate. Thus, LV diastolic filling is abnormal in a high percentage of patients with HCM, and verapamil normalizes or improves these abnormalities without altering systolic function. This mechanism may contribute to the clinical improvement of many HCM patients during verapamil therapy.

Adolescent↗
PubMed1979

Detection of early cardiac dysfunction in patients with severe beta-thalassemia and chronic iron overload.

To detect early left ventricular dysfunction, we used radionuclide cineangiography to determine left ventricular ejection fraction during exercise in 24 patients with transfusion-dependent, congenital anemias, 21 of whom had severe beta thalassemia. Ejection fraction at rest was normal in 21 patients (greater than 45 per cent) and in all patients was 53 +/- 2 per cent (mean +/- S.E.M.)--not significantly different from the value in normal subjects. However, ejection fraction during exercise was normal in only 11 patients (53 +/- 3 per cent in all patients, P less than 0.001 as compared with the normal value). All eight patients who had received fewer than 100 transfusions but only three of 16 (19 per cent, P less than 0.001) who had received 100 or more transfusions had normal responses during exercise. Whereas echocardiographic fractional shortening at rest was normal in 16 of 19 patients studied, eight patients with normal fractional shortening had abnormal ejection-fraction responses to exercise. Thus, radionuclide cineangiography during exercise is a highly sensitive technique for detecting preclinical myocardial dysfunction in patients with systemic iron overload.

Adolescent↗
PubMedDate not supplied

Three-dimensional intravascular ultrasonography: reconstruction of endovascular stents in vitro and in vivo.

BACKGROUND: Intravascular ultrasonography displays an artery in loosely related cross-sectional images with limited axial information. However, intravascular ultrasound images are suited to three-dimensional reconstruction. METHODS: A comprehensive intravascular ultrasound imaging system was used to reconstruct planar images in three-dimensions. This system consisted of a 25MHz transducer-tipped rigid probe (for in vitro studies) or a 25MHz transducer-tipped catheter within a 3.9F monorail imaging sheath (for in vivo studies), a motorized catheter pullback device that withdraws the transducer at 0.5mm/s, and an image processing computer that stacks 15 cross-sectional images/mm of stent axial length and then performs thresholding-based three-dimensional image rendering. We imaged 10 stents (4 Palmaz-Schatz, 3 Wiktor, 2 Strecker, and 1 Medinvent) in vitro after implantation in freshly harvested saphenous veins and 37 Palmaz-Schatz stents in vivo, 10 in native coronary arteries and 27 in vein grafts, 21 acutely and 18 on follow-up. RESULTS: Three-dimensional reconstruction of images obtained with this system reproduced the geometry of each stent design. In vitro, images of the Palmaz-Schatz stents showed the expanded diamonds, the central articulation, and flaring of both ends of both halves of the stents. Images of the Wiktor stents showed the sinusoidal wave-shaped coils in their helical configuration. Images of the Strecker stents showed the interlocking-loop design with gaps between the terminal loops at either end of the stent. Images of the Medivent stent reproduced the woven texture formed by braiding the stent wires. Three-dimensional reconstruction of images obtained in vivo also reproduced the spatial geometry of the Palmaz-Schatz stent. However, reconstruction of in vivo images was limited by cardiac-cycle-linked vessel motion and torsion and the presence of echo-dense tissue that could not be separated completely from the stent itself. CONCLUSIONS: Properly acquired intravascular ultrasound images can be used to reconstruct the spatial geometry of endovascular stents. Because stent spatial geometry is known and unambiguous, reconstruction of endovascular stents should be one of the tests of imaging systems designed to perform three-dimensional reconstruction of ultrasound images.

Adult↗
PubMedDate not supplied

Contemporary stent designs: technical considerations, complications, role of intravascular ultrasound, and anticoagulation therapy.

A number of studies have shown the benefits of stent placement over balloon angioplasty for the treatment of focal, native coronary artery, and saphenous vein graft disease. Although the number of stent designs available for clinical use has increased dramatically, the late clinical benefit of stenting over balloon angioplasty has yet to be shown in diffuse disease, complex bifurcation stenoses, or smaller (2.5-mm) vessels, each of which may require unique stent designs and adjunct therapies not currently available or extensively studied. The purposes of this review are to discuss the various stent designs currently available for clinical use, outline the known complications associated with these stents, assess the contribution of intravascular ultrasound, and describe current antiplatelet and antithrombotic therapy used after stent use.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Intracoronary radiation for patients with refractory in-stent restenosis: an analysis from the WRIST-Crossover Trial. Washington Radiation for In-stent Restenosis Trial.

BACKGROUND: In-stent restenosis (ISR) is a limitation of intracoronary stent implantation. In animal models and clinical trials, ionizing radiation has been shown to decrease in-stent neointimal formation. METHODS AND MATERIALS: In the Washington Radiation for In-stent Restenosis Trial (WRIST), patients with in-stent restenosis were first treated with conventional catheter-based techniques and then randomized to gamma irradiation (l92Ir, 15 Gy at 2 mm from the source) or placebo. Patients randomized to placebo that developed recurrent ISR and presented with anginal symptoms were crossed-over to active therapy. We compared the clinical and angiographic outcomes of 39 patients in the crossover group with 65 patients treated primarily with radiation. The primary clinical endpoints were mortality, morbidity, and repeat target lesion revascularization (TLR) at 6 months. RESULTS: Procedural success was 100%. In-hospital and 30-day complications were minimal. At 6 months, the rate for any multiple adverse cardiac events (MACE: death, MI, or TLR) was 25.6% in the crossover group vs. 29.2% in the primary treatment group (p = 0.86). Three patients in the crossover group and four in the primary treatment group died (p = NS). There were no Q-wave myocardial infarction. Ten (9.6%) of the patients presented with late thrombosis and total occlusion: 6.2% (4/65) in the primary treatment group vs. 15.4% (6/39) in the crossover group (p = 0.13). CONCLUSIONS: Patients who fail conventional catheter-based intervention without radiation can be treated with 192Ir with results similar to those who initially receive brachytherapy. This is of specific importance with respect to patients initially assigned to the placebo arm of randomized clinical trials.

Brachytherapy↗