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W J Corin

Publications and source records attributed to W J Corin.

14 recordsLinked to original sources
PubMed1992

Virtual real-time digital processing of hemodynamic data.

At present, the majority of cardiac catheterization laboratories acquire and store hemodynamic data in analog form. To examine the possibility of performing complex analysis of digital data during the catheterization procedure, we examined whether virtual real-time digital (fast Fourier) analysis improves the accuracy of clinical data. We compared digital filtering of fluid manometry during the right heart catheterization with 10-Hz and 250-Hz analog filters. Using the simultaneously acquired micromanometry as the "gold standard," we found that analog filtering is associated with a greater error and time delay than digital filtering. This study demonstrates that digital hemodynamic data analysis performed during cardiac catheterization can improve the quality of data obtained during right heart catheterization, with the results available within seconds. More extensive use of computers in the cardiac catheterization laboratory may be useful for both clinical and research purposes.

Atrial Function, Right↗
PubMed1992

Computer simulation of the effects of ventricular interdependence on indices of left ventricular systolic function.

The influence of ventricular interdependence on cardiovascular function has been convincingly demonstrated. In the intact cardiovascular system ventricular interdependence is always present, and thus measures of cardiac function include the contribution of ventricular interdependence (VI). A cardiovascular system model is presented and used to discuss how VI affects selected indices of left ventricular (LV) systolic function. Indices of LV function studied were the ejection fraction, stroke work, peak time derivative of ventricular pressure (dP/dT) and the LV end-systolic pressure-volume relationship. The effects of right ventricular (RV) volume through systolic VI on these indices are conveniently studied by comparing the model responses to pulmonary artery (PA) and vena caval (VC) occlusions; both PA and VC occlusion reduce LV volume, but the RV volume is increased by PA but reduced by VC occlusions. Through systolic VI the increase in RV volume with PA occlusion shifted the LV end-systolic pressure-volume relationship to the left and thus affected measures of LV maximum elastance. The LV ejection fraction, peak dP/dT and stroke work were all augmented by the increase in RV volume associated with the PA occlusion. Experimental studies comparing the responses to PA and VC occlusions are in broad agreement with the results described here. Systolic VI also shifted the cardiac function curve, a global measure of cardiac function, to the left. The results thus suggest that commonly used indices of LV systolic function are dependent on RV function and do not solely reflect LV function.

Cardiac Volume↗
PubMed1992

Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function.

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.

Animals↗
PubMed1991

Flosequinan: a vasodilator with positive inotropic activity.

Flosequinan is an oral arterial and venous vasodilator that is currently under investigation for the treatment of congestive heart failure. The effects of flosequinan on ventricular performance and myocardial contractility were studied in 10 patients with severe congestive heart failure during right and left cardiac catheterization. Sixty minutes after a 100 mg oral dose of flosequinan, the peak rate of rise in left ventricular pressure (dP/dt) increased from 940 +/- 180 to 1050 +/- 240 mm Hg/sec (p less than 0.05), while left ventricular end-diastolic pressure decreased from 32 +/- 5 to 26 +/- 8 mm Hg (p less than 0.05), and cardiac index increased (2.1 +/- 0.4 to 2.3 +/- 0.5 L/min/m2, (p less than 0.05). The mean pulmonary artery pressure and vascular resistance decreased from 40 +/- 8 to 33 +/- 12 mm Hg (p less than 0.05) and from 330 +/- 240 to 290 +/- 170 dyne-sec/cm5 (p less than 0.05), respectively. Heart rate, mean aortic pressure, right atrial pressure, systemic vascular resistance, and serum norepinephrine levels did not change significantly. The increase in left ventricular peak dP/dt that was concomitant with a decrease in left ventricular end-diastolic pressure, and no change in systemic arterial pressure or sympathetic tone, argue for a direct positive inotropic effect of flosequinan.

Adult↗
PubMed1991

Left ventricular passive diastolic properties in chronic mitral regurgitation.

BACKGROUND: In chronic mitral regurgitation, the myocardium responds to the increased filling volume by geometric alteration and eccentric hypertrophy. This study was designed to evaluate the effects of a pure volume overload on left ventricular diastolic chamber and myocardial properties and to assess the relation of passive diastolic function to systolic ejection performance. METHODS AND RESULTS: By use of simultaneous cineangiography and left ventricular micromanometry, left ventricular passive diastolic stiffness was evaluated in nine normal controls (group 1), 14 patients with chronic mitral regurgitation and a normal ejection fraction (greater than or equal to 57%, group 2), and 13 patients with mitral regurgitation and a reduced ejection fraction (less than 57%, group 3). Passive diastolic function was evaluated by using a three-constant elastic model. Left ventricular chamber properties were represented by the relation of pressure to volume; myocardial properties were evaluated by relating myocardial midwall stress to midwall strain. The constant of left ventricular chamber stiffness was decreased in group 2 compared with controls (p less than 0.05) but it was normal in group 3. The constant of myocardial stiffness was increased in group 3 compared with groups 1 and 2 (p less than 0.01). Among patients with mitral regurgitation, there was a significant inverse relation between ejection fraction and the constant of myocardial stiffness (r = -0.83). CONCLUSIONS: The chronic adaptation to volume overload in chronic mitral regurgitation tends to decrease left ventricular chamber stiffness. Patients with mitral regurgitation and a depressed ejection fraction demonstrated diastolic myocardial dysfunction. Compromised diastolic function in patients with chronic mitral regurgitation and reduced systolic performance may contribute to the clinical manifestations of congestive heart failure.

Adaptation, Physiological↗
PubMed1990

Myocardial stiffness derived from end-systolic wall stress and logarithm of reciprocal of wall thickness. Contractility index independent of ventricular size.

The slope of the end-systolic pressure-volume relation (ESPVR) is useful in assessing acute changes in contractile state. However, a limitation of ESPVR is that its slope decreases progressively as ventricular size increases without this change necessarily indicating a change in contractile state. In this respect, an index of contractile function that is independent of ventricular size would have an obvious advantage. The exponential constant (k) of the end-systolic relation between wall stress (sigma) and the natural logarithm of the reciprocal of wall thickness [ln(1/H)], sigma = Cekln(1/H), corresponds to the stiffness constant of the myocardium (kSM), a contractile index that should be independent of ventricular size and geometry. To examine the size independence of kSM, we studied left ventricular kSM during beta-blockade (to stabilize inotropic state) in 25 normal dogs with greatly differing ventricular sizes whose end-diastolic volumes ranged from 14 to 82 ml. The kSM was nearly constant (3.6 +/- 0.4) over this wide range of end-diastolic volumes and thus was independent of end-diastolic volume. Conversely, ESPVR, also obtained during beta-blockade, was closely and negatively correlated to end-diastolic volume (r = 0.92). To test the ability of kSM to measure changes in contractile state, we altered contractile state pharmacologically. The kSM increased from 3.7 +/- 0.5 to 4.8 +/- 0.8 (p less than 0.01) with infusion of dobutamine (after reversal of beta-blockade) and decreased to 3.1 +/- 0.3 (p less than 0.05) with inhalation of isoflurane, a negative inotrope, during beta-blockade (p less than 0.05). We conclude that kSM is independent of ventricular size and is sensitive to changes in inotropic state. As such, it should be useful as an index of contractile function.

Animals↗
PubMed1989

Abnormal subendocardial blood flow in pressure overload hypertrophy is associated with pacing-induced subendocardial dysfunction.

To detect the functional significance of subendocardial hypoperfusion in the pressure-overloaded left ventricle, we studied subendocardial and subepicardial function and subendocardial and subepicardial blood flow simultaneously in seven dogs with left ventricular hypertrophy (left ventricle/body weight ratio, 7.2 g/kg) produced by chronic aortic banding. Seven normal dogs served as controls. Subendocardial and subepicardial segment lengths were measured by ultrasonic dimension gauges, and myocardial blood flow was measured with radioactive microspheres. Atrial pacing (180-200 beats/min for 5 minutes) was used to produce a chronotropic stress. In dogs with left ventricular hypertrophy, the subendocardial blood flow failed to increase during pacing compared with the baseline state (1.21 +/- 0.17 vs. 1.22 +/- 0.17 ml/min/g). Subendocardial shortening fraction deteriorated with pacing stress (before pacing, 30.6 +/- 3.9%; after pacing, 24.2 +/- 3.7%; p less than 0.001). In controls, subendocardial blood flow increased from 1.32 +/- 0.19 to 1.80 +/- 0.19 ml/min/g during pacing, and shortening fraction was preserved (before pacing, 25.5 +/- 3.9%; after pacing, 25.9 +/- 3.3%). Subepicardial blood flow in dogs with hypertrophy increased from 1.54 +/- 0.24 to 2.32 +/- 0.34 ml/min/g, and subepicardial shortening fraction was maintained (before pacing, 10.4 +/- 1.0%; after pacing, 10.5 +/- 1.2%) as it was in controls (subepicardial blood flow, from 1.27 +/- 0.18 to 2.12 +/- 0.17 ml/min/g; shortening fraction, from 16.6 +/- 2.5% to 15.5 +/- 2.2%). We conclude that, with pacing stress in pressure-overload hypertrophy, subendocardial blood flow failed to increase. This abnormality corresponded with a deterioration in subendocardial contractile function.

Analysis of Variance↗
PubMed1989

Lacrimal catheterization.

A new atraumatic technique for identifying the medial cut end of a surgically lacerated canaliculus is described. It offers the advantage of allowing the surgeon to pass a stent through the canaliculus only, without surgically manipulating the lacrimal sac or nasolacrimal duct or damaging the ipsilateral canaliculus.

Basal Cell Carcinoma↗
PubMed1988

Abnormal exercise hemodynamics in patients with normal systolic function late after aortic valve replacement.

We studied the hemodynamic response to supine bicycle exercise in 20 patients late (10 +/- 2 years) after aortic valve replacement (for aortic stenosis in 12 patients, aortic insufficiency in six patients, and for combined stenosis and insufficiency in two patients). The pulmonary artery wedge pressure was obtained with a pulmonary artery balloon catheter, and left ventriculography was performed by digital-subtraction angiography after injection of radiographic contrast into the pulmonary artery. These patients were compared with 11 control subjects with no or minimal cardiac disease studied routinely for evaluation of chest pain in whom left ventricular end-diastolic pressure and a direct contrast ventriculogram were obtained. Compared with the control population, the study population had similar left heart filling pressures (7 +/- 3 vs 9 +/- 3 mm Hg, NS), but higher left ventricular ejection fractions (75 +/- 7% vs 67 +/- 7%, p less than .02) and higher left ventricular muscle mass indexes (106 +/- 28 vs 85 +/- 9 g/m2, p less than .01). Elevated myocardial muscle mass led to lower systolic wall stress in the study population than in the control subjects (254 +/- 65 vs 320 +/- 49 10(3).dynes/cm2, p less than .01) and might explain the higher ejection fraction observed. Fourteen patients had a normal response to exercise (with left heart filling pressures of 16 +/- 4 vs 18 +/- 2 mm Hg for control subjects, NS; and left ventricular ejection fraction of 77 +/- 8% vs 73 +/- 5% for control subjects, NS). However, while the remaining six patients had a normal exercise left ventricular ejection fraction (72 +/- 9%, NS), they had an abnormal rise in left heart filling pressure (33 +/- 8 mm Hg, p less than .01). Preoperatively these patients also had higher left ventricular mid- and end-diastolic pressures at similar diastolic volumes, suggesting a decrease in chamber compliance. Thus, late after aortic valve replacement there is a subgroup of patients who, despite normal hemodynamics and normal left ventricular systolic function as assessed by the left ventricular ejection fraction at rest, have an abnormal response to exercise characterized primarily by a substantial rise in left heart filling pressures. Preoperatively this group also has a decrease in diastolic chamber compliance despite nearly normal left ventricular ejection fractions. This abnormality appears to result from a primary derangement of diastolic function that is not evident at rest.

Aortic Valve↗
PubMed1988

Time course of regression of left ventricular hypertrophy after aortic valve replacement.

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 +/- 0.5 years), and late (8.1 +/- 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 +/- 73 to 105 +/- 35 ml/m2, p less than .01), a fall in left heart filling pressure (19 +/- 9 to 12 +/- 5 mm Hg, p less than .01), and maintenance of the cardiac index (3.3 +/- 0.8 to 3.5 +/- 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 +/- 13% to 64 +/- 10%, NS). By the late study the cardiac index (4.0 +/- 0.6 liters/min/m2, p less than .01) and left ventricular ejection fraction (66 +/- 15%, p less than .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 +/- 38 vs 120 +/- 29 g/m2, p less than .01), and a further 13% from the intermediate to the late study (105 +/- 32 g/m2, p less than .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 +/- 36 g/m2), and greater in those with aortic stenosis (158 +/- 33 g/m2) than in control subjects (85 +/- 9 g/m2, p less than .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 +/- 29 g/m2) and those with stenosis (114 +/- 27 g/m2) than in the control subjects (p less than .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium.

Aortic Valve↗
PubMed1988

Correction for preload in assessment of myocardial contractility in aortic and mitral valve disease. Application of the concept of systolic myocardial stiffness.

With single-beat analysis, the new concept of systolic myocardial stiffness is applied to provide a new approach for the assessment of myocardial contractility in aortic and mitral valve disease. Seventy patients underwent diagnostic right and left heart catheterization. Twenty-six patients had aortic stenosis, 18 had aortic insufficiency, and 26 had mitral regurgitation. Patients with aortic stenosis were divided into two groups on the basis of left ventricular mass index less than 172 g/m2 (AS1) and mass index greater than or equal to 172 g/m2 (AS2). The mitral regurgitation patients were divided into those in normal sinus rhythm (MR1) and those in atrial fibrillation (MR2). Nine patients without significant coronary or cardiovascular disease served as controls. Thirteen patients with aortic stenosis and eight with aortic insufficiency were evaluated (average, approximately 18 months) after successful aortic valve replacement. With simultaneous left ventricular pressure and cineangiographic methods, myocardial contractility was assessed by the conventional ejection fraction-afterload relation (uncorrected for preload) and by two new methods that permit the correction of the ejection fraction for preload. Assessments of the contractile state by these two new methods differed from those by the conventional method in 20-40% of the cases studied. Contractile state improved postoperatively in aortic stenosis and aortic insufficiency even in patients with preoperative depressed contractile states. In patients with mitral regurgitation, there was considerable heterogeneity of contractile function preoperatively. Severe left ventricular hypertrophy in aortic stenosis was not a marker for postoperative outcome since contractility was normal postoperatively in AS1 and AS2 in equal numbers. This study demonstrates that preload correction is important in a preoperative assessment of contractility in aortic and mitral valve disease but that it is less important postoperatively, presumably because of reductions in the preload.

Adult↗
PubMed1987

Is there coronary vasoconstriction after intracoronary beta-adrenergic blockade in patients with coronary artery disease.

Vasomotility of normal and stenosed coronary arteries was studied at rest and during supine bicycle exercise in 10 patients with classical exercise-induced angina pectoris receiving 1 mg intracoronary propranolol before the exercise test (propranolol group). Normal and stenotic coronary lumen areas were determined from biplane coronary arteriograms using a computer-assisted system. Measurements were performed at rest, after 1 mg intracoronary propranolol, during supine exercise (89 W for 3.4 minutes) and 5 minutes after 1.6 mg sublingual nitroglycerin administered at the end of the exercise test. The results were compared with previously obtained data on the effect of dynamic exercise on coronary lumen area in 12 patients receiving no medication (control group) and in 6 patients receiving 0.1 mg intracoronary nitroglycerin before the exercise test (nitroglycerin group). In the control group, coronary stenosis area decreased during exercise to 71% of levels at rest (p less than 0.001) whereas normal coronary lumen area increased to 123% of control (p less than 0.01). In the propranolol group both normal (113%, p less than 0.05 versus rest) and stenotic coronary lumen area (122%, p less than 0.05 versus rest) increased during exercise. A similar increase in both normal and stenotic areas was observed during exercise after pretreatment with 0.1 mg intracoronary nitroglycerin (123%, p less than 0.01 and 114%, p = NS versus rest). Sublingual administration of 1.6 mg nitroglycerin at the end of exercise increased coronary stenosis area to 145% (p less than 0.01 versus rest) in the propranolol group and to 115% in the control group (p = NS versus rest). It is concluded that intracoronary administration of propranolol does not potentiate coronary vasoconstriction of the epicardial vessels at rest and during exercise. In contrast, intracoronary propranolol prevents exercise-induced stenosis narrowing either because of reduced myocardial oxygen demand with a lower coronary blood flow resulting in a smaller transstenotic pressure gradient and, thus, a smaller flow-induced fall in stenosis distending pressure; or because of "local" beta-receptor blockade with unopposed distal arteriolar alpha-receptor tone, resulting in a higher poststenotic pressure and, thus, in a greater stenosis distending pressure; or because of a local anesthetic effect of propranolol with a decrease in calcium influx to the coronary smooth musculature.

Adult↗
PubMedDate not supplied

Voltage-dependent performance of skeletal muscle pouches: implications for cardiomyoplasty.

Cardiomyoplasty, a new therapy for heart failure, uses autologous skeletal muscle to mechanically assist the heart. The success of dynamic cardiomyoplasty is critically dependent on the contraction strength of the assisting skeletal muscle. Unlike cardiac muscle, skeletal muscle contracts in a graded response to electrical stimulation. However, in current cardiomyoplasty practice, no systematic technique exists to set the stimulating voltage effecting skeletal muscle contraction. The stimulating voltage is simply set to some multiple of the "threshold" voltage. Furthermore, researchers do not consider the role of stimulating voltage when they determine the amount of assistance afforded during cardiomyoplasty. To more accurately assess the value of this heuristic voltage-setting technique, we investigated the role of stimulating voltage on the strength of contraction of the latissimus dorsi muscle. Six New Zealand white rabbits had isovolumic hydraulic pouches constructed from the latissimus dorsi muscle. The muscles were wrapped around a compliant balloon in which isovolumic pressure development was measured during tetany-inducing burst (pulse-train) stimulation. The tetanic plateau of the pouch pressure record was used to measure the effects of stimulating voltage on skeletal muscle contraction. Results indicated that (1) increasing stimulating voltage from two to four times the "threshold" voltage increased normalized pouch pressure from 0.38 +/- 0.21 to 0.78 +/- 0.12 (mean +/- SD) (p < 0.05); (2) the threshold-normalized voltage necessary to cause maximal muscle contraction varied widely (5.7 +/- 2.0, mean +/- SD; range, 3.1 to 9.3); and (3) the current achieving maximal pressure development varied from 5.6 to 31.4 mA (19.9 +/- 10.4 mA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗