Reduction In Systolic Function Research Articles

The effect of ageing, hypertension and its treatments on regional myocardial function

Hypertension and ageing cause impaired diastolic function. Tissue Doppler echocardiography (TDE) enables assessment of regional myocardial diastolic and systolic function. An application of this is the detection of myocardial ischaemia where regional abnormalities would be expected to occur in the territory supplied by an affected coronary artery. In order for TDE to be useful in the detection of ischaemia, other pathologies and treatments should not cause similar changes. 48 subjects comprising 4 equal matched groups: younger normals (mean age 36), older normals (mean age 55), hypertensives treated (without β-blockers) and hypertensives treated (with β-blockers) were studied. TDE was performed from the apical window: velocities were measured at the tricuspid annulus(T)of the right ventricle, and from the septal(Se), lateral(L) and inferior(I) mitral annuli of the left ventricle. These correspond to territories supplied by the left anterior descending, circumflex and right coronary arteries respectively. Mean systolic (S) velocities in cm/s and E/A ratios. (See Table). p<0.05 vs.Y p<0.01 vs.Y p<0.05 vs.N p<0.05 vs.Y p<0.01 vs.Y p<0.05 vs.N The E/A ratios were reduced in both the hypertensive and age-matched older normotensives. Ageing and hypertension cause reductions in right and left ventricular diastolic function and these changes occur homogeneously. β-blockade causes a homogeneous reduction in systolic function. The effects of age, hypertension and treatment with β-blockers would not preclude the detection of myocardial ischaemia, which causes regional abnormalities, by TDE in this group of patients.

Pharmacodynamics of propranolol on left ventricular function: Assessment by Doppler echocardiography

The relationship of left ventricular systolic function and heart rate to serum l-propranolol concentrations was determined in 10 healthy male volunteers during maximal exercise treadmill testing. Peak aortic blood flow acceleration (ACL), measured by Doppler ultrasonography, was used to evaluate left ventricular systolic function. Repeated exercise testing was performed on two separate days after long-term oral administration of 40 mg propranolol or placebo every 6 hours in a randomized, double-blind, crossover fashion. Pharmacodynamic relationships were determined by fitting percent change in ACL and heart rate at maximal exertion with 1-propranolol with the Emax model (maximal effect) and nonlinear regression. Reductions in systolic function and heart rate during exercise were related directly to 1-propranolol. Propranolol was significantly (p less than 0.05) more potent in reducing heart rate (EC50, 10.6 +/- 9.2 ng/ml) compared with ACL (EC50, 19.2 +/- 8.9 ng/ml). However, Emax of propranolol for reducing ACL was significantly greater than that for reducing heart rate (-46.7% +/- 6.9% versus -29.5% +/- 15.9%; p less than 0.05). These data indicate that the concentration-effect relationship for 1-propranolol and its negative inotropic effect differ from its negative chronotropic effect.

EFFECT OF VERAPAMIL ON CANINE LEFT VENTRICULAR FUNCTION IN THE PRESENCE OF FENTANYL WHEN APICAL BLOOD FLOW IS CRITICALLY LIMITED

Instruments were inserted to seven dogs under halothane anaesthesia, to measure global and regional left ventricular function. Anaesthesia was continued with fentanyl (100 micrograms kg-1 bolus, then 1.5 micrograms kg-1 min-1). Critical constriction was applied to the left anterior descending coronary artery. Control recordings were made, followed by bolus administration of verapamil 0.08, 0.16 and 0.32 mg kg-1, with recordings 10 min after each bolus. At the highest dose, verapamil decreased systemic arterial pressure, left ventricular dP/dt, stroke volume and systemic vascular resistance, and increased heart rate significantly. Coronary perfusion pressure decreased and, in the presence of critical constriction, coronary flow per beat decreased significantly. In the region with constriction, systolic shortening of myocardium decreased and post-systolic shortening increased significantly with addition of verapamil. The addition of a high dose of verapamil to fentanyl anaesthesia caused reduction in systolic function and development of early diastolic dysfunction in myocardium with critically limited blood supply.

Myocardial performance after arterial switch operation for transposition of the great arteries with intact ventricular septum.

Left ventricular dimensions, wall thickness, wall stress, and indexes of afterload, preload, contractility, and early diastolic function, as well as regional wall motion, were determined by echocardiographic methods in patients with transposition of the great vessels after arterial switch operation and in age-matched normal controls. In patients evaluated early after surgery, body surface area-adjusted left ventricular dimensions were smaller, and wall thickness was increased compared with controls. Ventricular performance (fractional shortening) was normal in most patients but was abnormally low in 10%. Nevertheless, contractility was normal or augmented in all subjects, with a mean value higher than the control group. The reduction in systolic function was related to altered loading conditions with a combination of reduced afterload and preload combined with augmented contractility. These altered myocardial mechanics appeared to be secondary to routine therapy with digitalis and diuretics. Diastolic function was also normal with differences in the rate of peak filling and rate of wall thinning entirely attributable to differences in ventricular size and function, and normalized indexes of diastolic function were not different between patients and controls. Patients evaluated late after repair were found to have normal regional wall motion with no evidence to suggest regional dysfunction as might be seen with regional ischemia. Ventricular size, wall thickness, systolic function, afterload, preload, contractility, and early diastolic function were indistinguishable from control values. Indexes of diastolic function demonstrated the same relation to age, body surface area, and ventricular size and function in both patients and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of insulin and glucagon on systolic properties of the normal and septic isolated rat heart.

Controversy exists in the literature concerning the effects of insulin and glucagon on cardiac muscle contractility, in particular during anoxia, ischemia or sepsis. The purpose of the present study was to determine the effects of insulin and glucagon on the systolic function of the normal and the dysfunctioning septic rat myocardium in the Langendorff preparation. In the normal isolated rat heart, neither insulin nor glucagon exhibited any lasting inotropic effect on systolic function or coronary flow. Sepsis (cecal ligation and puncture) resulted in a dramatic reduction of systolic function to 44% of control animals. All insulin-containing formulations tested improved systolic function in septic hearts by a mean of 85% compared to Krebs and glucose only. However, this improvement did not reach statistical significance compared to the use of Krebs and glucose only. Glucagon at 100 micrograms/l was doing as well as Krebs and glucose alone while at 1 mg/l glucagon was only able to maintain pre-perfusion contractility. Our results suggest that neither insulin nor glucagon seem to possess special inotropic properties for the isolated perfused normal or septic rat heart.