Left Ventricular Fiber Shortening Research Articles

Increased left ventricular contractility during cross-clamping of the descending thoracic aorta

To evaluate how left ventricular (LV) dimensions and contractility and proximal systemic hemodynamics respond during and after 30 minutes of cross-clamping of the descending thoracic aorta. The study was prospective and controlled. The study was performed in a university animal laboratory. Ten pigs (bodyweight: 22 to 30 kg). The pigs were anesthetized with fentanyl and ketamine, and the heart and aorta were exposed through a left thoracotomy. The aortic root pressure and flow and LV dimensions were monitored with a high-fidelity pressure catheter, a precalibrated ultrasonic transit-time flow probe, and by two-dimensional ultrasound imaging, respectively. After 1 minute of cross-clamping, LV end-diastolic and end-systolic diameters were increased 17% and 32% above baseline (both p < 0.001), respectively, whereas LV fiber shortening was decreased by 35% (p < 0.05) corresponding to the 257% increase in wall stress (p < 0.001). After 5 minutes, LV dimensions, fiber shortening, and wall stress had returned to baseline levels. After 10 minutes, fiber shortening was increased 67% (p < 0.05), although wall stress was maintained at baseline levels. Simultaneously, the aortic mean blood pressure, heart rate, and cardiac output peaked 112% (p < 0.001), 81% (p < 0.001), and 125% (p < 0.01) above baseline, respectively. Cross-clamping grossly increased systemic afterload grossly and was followed by moderate LV dilation, which resolved after 5 minutes owing to the combined effects of proximal vasodilation, increased myocardial contractility, and tachycardia. This hyperdynamic circulatory state was maintained during cross-clamping and decreased after declamping.

The effects of donor-recipient size disparity in infant and pediatric heart transplantation

To determine the effect of heart donor and recipient size mismatches in infant and pediatric heart transplantation, we studied all 69 patients (age 1 day to 11 years) having 71 orthotopic heart transplants from 1985 to 1989. Patients were divided into three groups based on donor to recipient weight ratios. Group I comprised 13 heart transplants with a donor to recipient weight ratio less than 0.95 (mean 0.81, range 0.48 to 0.94); group II comprised 29 heart transplants with a weight ratio between 0.95 and 1.60 (mean 1.28); and group III had 27 heart transplants with weight ratios greater than 1.60 (mean 2.2, range 1.61 to 3.09). All chests were closed primarily. The cardiothoracic ratio by chest radiography was significantly larger in group III (p = 0.0002); 75% of group III patients had periods of lobar or complete lung collapse by chest radiography compared with 28% of group II and 19% of group I patients (p < 0.05). Despite this, there was no difference in the number of days of ventilator support for any group (p = 0.92). There was no difference in graft ischemic time or inotropic drug use among groups, nor were differences found in the cardiac systolic function parameters of left ventricular preejection time (p = 0.975), left ventricular ejection time (p = 0.975), left ventricular fiber shortening (p = 0.97), and left ventricular fractional shortening (p = 0.596). Thus despite a high incidence of transient lobar or complete lung collapse in high donor to recipient weight ratio transplants, large donor heart size produces very little clinical impairment in recipient lung function. Size mismatches do not influence cardiac systolic function. Overall, large size mismatches appear to be very well tolerated in infant and pediatric heart transplantation.

Vasodilator Therapy for Chronic Congestive Heart Failure

THE USE of vasodilators as adjunctive therapy for congestive heart failure was first popularized over ten years ago by the work of Parmley, Chatterjee, Cohn, and Franciosa, although occasional clinical investigative reports using vasodilators date back to the 1950s and even earlier. Physicians have had considerable experience with vasodilators, yet important questions remain unanswered regarding the ultimate role of this therapeutic approach to the failing heart. This review will focus on the present status of the currently available vasodilators (nitrates, hydralazine hydrochloride, prazosin hydrochloride, and captopril) in the management of chronic congestive heart failure. THE CONCEPT OF VASODILATOR THERAPY Afterload or Impedance Reduction Afterload, a term derived from isolated cardiac muscle experiments, is best defined as the forces opposing left ventricular fiber shortening during ejection.Impedance, a term preferred by many investigators, is the instantaneous resistance to flow to the contracting left ventricle and is equivalent to instantaneous left ventricular

Vasodilator therapy for chronic congestive heart failure

THE USE of vasodilators as adjunctive therapy for congestive heart failure was first popularized over ten years ago by the work of Parmley, Chatterjee, Cohn, and Franciosa, although occasional clinical investigative reports using vasodilators date back to the 1950s and even earlier. Physicians have had considerable experience with vasodilators, yet important questions remain unanswered regarding the ultimate role of this therapeutic approach to the failing heart. This review will focus on the present status of the currently available vasodilators (nitrates, hydralazine hydrochloride, prazosin hydrochloride, and captopril) in the management of chronic congestive heart failure. <h3>THE CONCEPT OF VASODILATOR THERAPY Afterload or Impedance Reduction</h3> <i>Afterload</i>, a term derived from isolated cardiac muscle experiments, is best defined as the forces opposing left ventricular fiber shortening during ejection.<i>Impedance</i>, a term preferred by many investigators, is the instantaneous resistance to flow to the contracting left ventricle and is equivalent to instantaneous left ventricular

Adverse cardiac effects of acute alcohol ingestion in young adults.

Previous studies of the effects of acute alcohol ingestion in normal subjects have used measures of left ventricular performance that are altered by changes in preload and afterload and in contractile state. In studies involving nine healthy, young adults, we measured sensitive load-independent end-systolic indices of left ventricular contractility over a wide range of pressures generated by methoxamine infusion before and after oral alcohol administration. Echocardiography was used in conjunction with calibrated carotid pulse tracings. Alcohol ingestion resulted in a fall (p less than 0.01) in left ventricular end-diastolic dimension (a measure of preload), end-systolic wall stress (a measure of afterload), and systemic vascular resistance, while not changing the left ventricular shortening fraction. In contrast, the end-systolic pressure-dimension slope decreased (p less than 0.001) and the rate-corrected velocity of left ventricular fiber shortening at an end-systolic wall stress of 50 g/cm2 fell (p less than 0.001). Thus, when load-independent assessment of left ventricular contractility is done, acute alcohol ingestion has a myocardial depressant effect greater than previously suspected.

Left ventricular end-systolic wall stress-velocity of fiber shortening relation: A load-independent index of myocardial contractility

The velocity of circumferential fiber shortening (Vcf) is an index of myocardial performance which, although sensitive to contractile state, has limited usefulness because of its dependence on left ventricular loading conditions. This study investigated the degree and velocity of left ventricular fiber shortening as it relates to wall stress in an attempt to develop an index of contractility that is independent of preload and heart rate while incorporating afterload. Studies were performed in 78 normal subjects using M-mode echocardiography, phonocardiography and indirect carotid pulse tracings under baseline conditions. In addition, studies were performed on 25 subjects during afterload augmentation with methoxamine, 8 subjects before and during afterload challenge after increased preload with dextran and 7 subjects with enhanced left ventricular contractility with dobutamine. The relation of end-systolic stress to the velocity of fiber shortening and to the rate-corrected velocity of shortening (corrected by normalization to an RR interval of 1) was inversely linear with correlation coefficients of -0.72 and -0.84, respectively. Alterations in afterload, preload or a combination of the two did not significantly affect the end-systolic wall stress/rate-corrected velocity of shortening relation, whereas during inotropic stimulation, the values were higher, with 94% of the data points above the normal range. Age did not appear to affect the range of normal values for this index. In contrast, the end-systolic wall stress/fractional shortening relation was not independent of preload status, responding in a manner similar to that seen with a positive inotropic intervention. Thus, the velocity of circumferential fiber shortening normalized for heart rate is inversely related to end-systolic wall stress in a linear fashion. Accurate quantitation can be performed by noninvasive means and a range of normal values determined. This index is a sensitive measure of contractile state that is independent of preload, normalized for heart rate and incorporates afterload. In contrast, the end-systolic wall stress/fractional shortening relation is dependent on end-diastolic fiber length in the range of physiologically relevant changes in preload.

Assessment of left ventricular contractility in patients receiving doxorubicin.

The usual indices of left ventricular systolic performance have been incapable of accurately recognizing early myocardial impairment in many patients treated with doxorubicin. Recently, several new load-independent, highly sensitive indices of left ventricular contractility have been developed including the slope value of the endsystolic pressure (Pes)-dimension (Des) relation and the position of the left ventricular end-systolic wall stress (sigma es)-percent fractional shortening (% delta D) relation. We used these indices to study 46 patients receiving either low dose or high dose doxorubicin. Results were compared with data from 30 healthy subjects. Resting % delta D failed to accurately recognize left ventricular dysfunction in 9 of 17 patients with low normal values. These patients had reduced afterload, as measured by sigma es, permitting normal extent of left ventricular fiber shortening despite impaired contractility as quantified by diminished Pes-Des slope values. There was 98% concordance between the relative position of the sigma es-% delta D relation and the slope value of the Pes-Des, relation. These indices offer an improved means of recognizing and quantitating impaired contractility in patients treated with doxorubicin.

Intra-aortic Balloon Counterpulsation in an Experimental Model of Myocardial Infarction

The efficacy of intra-aortic balloon counterpulsation for heart failure during acute myocardial infarction has been controversial, and early intervention has been suggested as crucial. We have examined this type of therapy in the intact anesthetized dog during complete occlusion of the proximal left anterior descending coronary artery with a balloon-tipped catheter. Group 1 (n = 8) represented untreated animals undergoing four hours of ischemia. Group 2 (n = 7) consisted of animals undergoing counterpulsation with an intra-aortic balloon after 15 minutes of ischemia. Initially, stroke volume and the mean rate of left ventricular fiber shortening were similarly diminished in both groups, while filling pressure rose proportionately. After four hours, the mean rate of fiber shortening, stroke volume, and left ventricular filling pressure rose to a greater extent in untreated compared to treated animals (p less than 0.01). The degree of swelling in ischemic tissue and the number of sites with ST-segment elevation and their sums were comparable in the two groups. Thus, intra-aortic counterpulsation applied early in the course of ischemia can improve global left ventricular dysfunction without affecting the extent of myocardial injury.

Comparative cardiac dynamic effects of dobutamine and isoproterenol in conscious instrumented dogs

The cardiac dynamic consequences were evaluated of constant infusions of dobutamine and isoproterenol at graded dose levels into conscious, healthy instrumented dogs. Measurements were made of simultaneous changes in left ventricular internal diameter, pressure, aortic pressure and rate of rise of left ventricular pressure (dP/dt), as well as the left ventricular electrogram. From these primary variables, derived variables were computed using programs in a minicomputer system. The data showed that, with increasing doses of dobutamine there were significant linear increases in all measured indexes of myocardial contractility, such as the rate of rise of left ventricular pressure at a developed isovolumic pressure of 40 mm Hg (dP/dt/P40), mean velocity of left ventricular fiber shortening, ejection fraction and stroke work. These changes in myocardial contractility occurred without changes in end-diastolic volume, mean aortic pressure or heart rate when dobutamine was infused in doses of 5 to 20 μg/kg per min. Isoproterenol also produced linear changes in indexes of myocardial contractility but in doses of 0.02 to 0.10 μg/kg per min, it produced a significantly higher heart rate at any given level of contractility than that produced by dobutamine. Cardiac minute work (heart rate × stroke work) was increased by both drugs. However, with infusions of isoproterenol the amount of cardiac minute work was significantly limited because of the changes in heart rate, whereas with dobutamine cardiac minute work could be increased to a higher level as a function of changes in myocardial contractility alone without changes in heart rate. These data suggest that dobutamine selectively increases myocardial contractility.