Index Of Myocardial Contractility Research Articles

Left ventricular function in hypothyroidism. Responses to exercise and beta adrenoceptor blockade.

The effects of exercise and beta adrenoceptor blockade on left ventricular function were assessed in eight patients with hypothyroidism before and during thyroxine replacement treatment. Left ventricular ejection fraction, measured by radionuclide ventriculography, was reduced in hypothyroid patients at rest and on exercise. The rise in ejection fraction with exercise was, however, similar in both groups. Pretreatment with intravenous propranolol reduced the ejection fraction at rest 9% in both hypothyroid and euthyroid patients and reduced the rise on exercise. Directional changes in a second index of myocardial contractility based on the shape of the ventricular volume curve paralleled the changes in the ejection fraction. Left ventricular function is therefore reversibly depressed by thyroid hormone deficiency but responses to exercise and beta adrenoceptor blockade are normal. There is no evidence of altered adrenergic sensitivity in the control of myocardial contractility in hypothyroidism.

Cold blood potassium cardioplegia: Effects of increasing concentrations of potassium

The optimal levels of potassium for cardioplegia have been reported to be 13 to 40 mEq/L, although 24 hour preservation of the heart has been achieved with 120 ± 6 mEq/L and Melrose described use of 245 mEq/L. Five groups of six dogs each had 1 hour of myocardial ischemia with a systemic temperature of 27° ± 2° C and a myocardial temperature of 7° ± 2° C (crushed ice) after coronary perfusion with 200 ml of blood (6° ± 2° C at 70 mm Hg) containing various concentrations of potassium chloride: 30 mEq/L (K-30), 60 (K-60), 120 (K-120), or 240 mEq/L (K-240). One group (2K-30) had perfusion with 400 ml of cold blood containing potassium chloride, 30 mEq/L. Baseline studies were repeated after 40 minutes of reperfusion and warming to 37.5° ± 0.5° C. Peak systolic pressure declined in K-60 and K-240 dogs. Indices of myocardial contractility (V max , V ce , and dp/dt) declined in K-240 hearts. Left ventricular compliance and muscle stiffness did not change. Heart water and coronary vascular resistance were unchanged. Total coronary flow was elevated during reperfusion in K-30 and 2K-30 hearts but was unchanged in the others. Myocardial oxygen consumption was increased throughout reperfusion in K-30 hearts and was depressed during early reperfuson in K-60, K-120, and K-240 hearts. Lactate uptake was reduced during early reperfusion in all groups except 2K-30. Myocardial biopsy specimens revealed a 70% to 82% decline in creatine phosphate with return to control during reperfusion in all groups. Adenosine triphosphate (ATP) did not fall with ischemia but did so with reperfusion in K-60 and K-120 hearts. Ultrastructurally, there was focal myofibrillar injury in all groups. Two lesions, (1) capillary endothelial bleb formation and (2) intracellular vacuolization, were present in K-60, K-120, and K-240 hearts but were not progressive. The relative lack of injury related to increasing potassium concentrations is related to the use of profound hypothermia.

Assessment of myocardial performance in ischaemic heart disease: from changes in left ventricular power output produced by graded-dose isoprenaline infusion.

Current clinical indices of myocardial contractility derive from concepts of muscle mechanics developed from isolated muscle experiments. Numerous simplifying assumptions are needed to apply these concepts to contractility studies in the whole heart. An alternative is to consider the heart as a pump which generates both pressure (P) and flow (Q) and to estimate its performance from the power output of its ventricles (P X Q). A method is described for measuring peak left ventricular power output in patients during routine cardiac catheterisation. The measurements have been made at rest and following inotropic challenge with gradient infusions of isoprenaline intravenously. Results from 13 patients with coronary artery disease and severe angina pectoris, who were clinically indistinguishable from one another, are reported. The patients could be grouped according to their left ventricular peak power responses to isoprenaline, although no difference could be demonstrated between them at rest. The patients who showed no increase in left ventricular power response to isoprenaline had a poor prognosis.

Effects and mechanism of action of aminophylline on cardiac function and regional blood flow distribution in conscious dogs.

The effects of aminophylline, 1 mg/kg/min infused intravenously for 10 minutes, were examined on left ventricular (LV) diameter, pressure, an indexes of myocardial contractility, as well as systemic, coronary and regional hemodynamics in conscious dogs. Aminophylline increased mean arterial pressure 12 +/- 2%, LV systolic pressure 8 +/- 1%, LV dP/dt 20 +/- 2%, velocity of myocardial fiber shortening 13 +/- 2% and heart rate 5 +/- 2%, and reduced LV end-diastolic diameter 2 +/- 0.5%. Vascular resistance rose in the systemic bed 13 +/- 5%, the coronary bed 26 +/- 3%, the mesenteric bed 26 +/- 5% and the iliac bed 36 +/- 4%, but did not rise in the renal bed. Both beta-adrenergic receptor blockade with propranolol and chronic treatment with reserpine attentuated but did not abolish the positive inotropic response induced by aminophylline. Alpha-adrenergic receptor blockade with phentolamine prevented aminophylline-induced vasoconstriction in the systemic, coronary, mesenteric and iliac beds. In contrast to the vasoconstriction with i.v. aminophylline, when the drug was infused directly into the iliac artery, it elicited marked iliac vasodilation. Thus, in the intact conscious dog, i.v. aminophylline, in a dose that had little effect on heart rate, increased LV contractility and reduced preload. The increase in contractility was dependent in part on intact beta-adrenergic nervous activity and endogenous catecholamine stores. The increase in systemic, coronary, iliac and mesenteric resistances involved alpha-adrenergic mechanisms. These actions appear to involve autonomic mechanisms, because the only direct effect of aminophylline on the iliac artery was marked vasodilation.

Cardiac function in primary hypothyroidism.

Cardiac chamber dimensions and myocardial function were studied in 15 children with primary hypothyroidism prior to and after thyroxine therapy. Small pericardial effusions were detected in 11 of 15 subjects before therapy, which resolved in nine of 11 subjects after initiation of thyroxine replacement. There was no association between the severity of the thyroid failure and the presence of effusion, and no evidence of cardiac compromise due to effusions. No significant abnormality in cardiac chamber or myocardial dimensions, systolic time intervals, or indices of myocardial contractility was detected among the hypothyroid children as compared with a normal population. Neither myocardial dimensions nor contractility indices changed significantly on reestablishment of normal thyroxine concentrations with exogenous hormone. These data refute the existence of a myocardiopathy associated with hypothyroidism in children.

The heart in chronic alcoholism: a noninvasive study

The echocardiogram and systolic time intervals were used to evaluate cardiac function in 73 chronic alcoholic subjects without symptoms of heart disease. All were below the age of 45 years and none had arterial hypertension or history of heart disease. The echocardiograms of chronic alcoholic individuals revealed increased thickness of the left ventricular wall (10.4 mm. ± 1.05, normal controls 8.76 mm. ± .86, p < 0.001), interventricular septum (11.71 mm. ± 1.33, normal controls 9.63 ± 1.24, p < 0.001) and markedly increased left ventricular mass (145 gm./M. 2 ± 32, normal controls 101 ± 20.7, p < 0.001). The echocardiographic indices of myocardial contractility (ejection fraction, wall excursion and velocity, circumferential fiber shortening) were normal. Systolic time intervals revealed shortening of ejection time and prolongation of the pre-ejection period. It was found that approximately half of the asymptomatic alcoholic subjects have left ventricular hypertrophy without echocardiographic evidence of decreased myocardial contractility. It is suggested that abnormal systolic time intervals may be due to decreased myocardial compliance.

Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H2O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial cointractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload.

Effects of Relaxation Therapy on Cardiac Performance and Sympathetic Activity in Patients with Organic Heart Disease

Six patients, with surgically implanted tantalum myocardial markers, were trained in deep muscle relaxation therapy. Analysis of individual responses and group means of blood pressure and ventricular dimensions during relaxation showed a decrease in plasma norepinephrine levels and indices of myocardial contractility compared to the control state. Heart rate changes in individuals during relaxation were directly correlated with changes in plasma norepinephrine levels, although group means for heart rate did not change significantly between control and relaxation periods. Base-line plasma norepinephrine levels were directly correlated with systolic blood pressure and were inveresly correlated with a measure of myocardial contractility. These data suggest that physiological changes during relaxation may be mediated through the sympathetic nervous system.

Antihypertensive polar renomedullary lipid, a semisynthetic vasodilator.

Two types of biologically active lipids have been derived from renomedullary tissue. One is neutral (ANRL) and the other polar (APRL). Upon a bolus I.V. injection, APRL causes a rapid decline of the mean arterial pressure (MAP) after a single injection and a prolonged depressor effect after either multiple injections or an infusion. APRL became evident when a reduction procedure, using the Vitride reagent, was used. Thus, APRL is likely a semisynthetic product. Multiple chemical and enzymatic manipulations suggest that APRL is a glycerophosphate with the active acyl group in Position 2. The acute and prolonged effects of APRL may be due to different components in its mixture. Hemodynamic studies indicate that both the acute and prolonged effect of APRL causes vasodilatation with minimal or no tachycardia. Visualization of the microcirculation reveals arteriolar dilatation. Larger bolus doses also cause a decrease in cardiac output (CO) that could be due to venodilatation. A negative i DO tropic effect has not been ruled out for APRL. This seems unlikely as indicated by minimal change in CO as MAP is lowered substantially (lower doses), no change in right atrial pressure, no direct effect on isolated atria] myocardium and no change in the index of myocardial contractility. It is suggested that the depression of CO with higher doses may be due to venodilatation. Preliminary studies fail to reveal acute toxiclty. APRL is a powerful vasodilator. (Hypertension 1: 299-308, 1979)

Systolic Time Intervals, Hemodynamics, and Indices of Myocardial Contractility in Normal Koreans

Systolic Time Intervals, Hemodynamics, and Indices of Myocardial Contractility in Normal Koreans

The effect on myocardial contractility of a new beta-adrenergic receptor blocking drug, penbutolol.

1 The inotropic effect of penbutolol, a new beta-adrenergic receptor blocking drug, has been compared with that of propranolol in two similar groups of six subjects each. 2 Inotropic changes were assessed from changes in myocardial contractility index [LV dp-dt/11 T] as well as the slope of the regression line relating LV dp/dt to LVED during incremental pacing. 3 Penbutolol was found to have a significant negative inotropic effect of an order similar to that of propranolol in the respective doses studied.

Cardiovascular function in dogs with acute hypokalemia.

The effects of acute hypokalemia on plasma electrolytes, cardiovascular function, osmolality, and hematocrit were investigated in anesthetized dogs for 2 hours. There was progressive increase in the total systemic vascular resistance, but no change in the osmolality and blood hematocrit. All of the hemodynamic parameters decreased except the preferred index of myocardial contractility, [dp/dt]/IIP, which increased during hypokalemia. The changes in this index of myocardial contractility were associated with changes in the plasma potassium but not the plasma sodium. The results suggest that hypokalemia-induced increases in myocardial contractility might be associated with an increased influx of Ca++ as a result of hypokalemia-induced inhibition of sarcolemmal Mg++ -dependent, Na+-K+-ATPase.

134 PRE-AND POST-OPERATIVE RIGHT VENTRICULAR VOLUME &amp; FUNCTION CHARACTERISTICS IN TETRALOGY OF FALLOT

Right ventricular volume and function characteristics were evaluated in 25 pre-operative and 28 post-operative patients aged 10 days to 24 years. Pre-operative patients were grouped according to the pulmonary-to-systemic flow ratio (Qp/Qs) and post-operatively according to magnitude of right ventricular (RV) peak pressure (pr.) and residual pulmonary-to-RV pressure gradients (Δ PA-RV). Pre-operatively: cardiac index (CI) was highest and pulmonary index (PI) was lowest in those with smallest Qp/Qs; RV end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV) and ejection fraction (EF)were all mildly depressed but not significantly different in various Qp/Qs groups. RV myocardial contractility index (MCI) approached normal for a systemic ventricle. Stroke work (SW) was lowest in patients with palliative left-to-right shunts (LRS). Post-operatively: EDV and ESV were elevated but highest in patients with high residual RV pr. or large Δ PA-RV. SV was normal. EF was depressed in all groups, being lowest in those with highest RV pr. or Δ PA-RV. SW and MCI were normal in low RV pr. RV outflow aneurysms were identified in 3/10 patients in the low RV pr. group and in 12/16 with highest residual pr. The incidence of pulmonary regurgitation (PR) was similar in each group. We conclude that post-operatively in patients with tetralogy of Fallot: (1) significant RV dysfunction persists being worst in those with high residual RV pr. and Δ PA-RV; (2) dysfunction is related to the incidence of RV outflow aneurysm and PR; and (3) elevated ESV results from large aneurysms with small diastolic to systolic volume change.

MYOCARDIAL STIMULATION BY PANCURONIUM BROMIDE

The effect of pancuronium bromide on the canine myocardium was studied by observing several indices of myocardial contractility during i.v. and intracoronary infusion of the drug in an anaesthetized, open-chested dog preparation. Pancuronium produced tachycardia when given for 2 min by i.v. and intracoronary infusion with the heart intact. Following denervation and pacing of the heart the intracoronary infusion of the drug produced increases in maximum acceleration of blood at the aortic root, peak aortic blood flow, maximum dP/dt and (maximum dP/dt)/TP. These changes occurred about 30 s after starting the infusion and returned to control values 5 min after stopping the infusion.

133 HEMODYNAMIC AND LEFT VENTRICULAR VOLUME AND FUNCTION CHARACTERISTICS IN THALASSEMIA MAJOR (Thal)

Hemodynamic and left ventricular (LV) volume and function characteristics obtained at cardiac catheterization were evaluated in 12 patients with Thal aged 11-28 years (mean 20.4 years) and compared to values in 17 normal subjects.At the time of study, hemoglobin was 10.9 ± 1.6 Gm%.Right atrial and ventricular (RV), and pulmonary artery and wedge pressures were normal.LV and aortic pressures and RV and LV dP/dt were normal.Oxygen consumption [220.7 ± 47.5 cc/min] and cardiac index (Qs) [4.9 ± 0.8 Lit/min/M2] were normal.LV end-diastolic (EDV) and end-systolic (ESV) volumes were increased [138.4 ± 38.9%, p< 0.01; 183.1 ± 49.5%, p< 0.001 respectively] . Stroke volume, however, remained normal, as did forward flow and stroke work. Ejection fraction (EF) was significantly reduced [90.7 ± 7.1%, p< 0.01] . Myocardial contractility index, Mass and VCF were not altered. Left atrial maximal volume (LAMV) was significantly increased [140.1 ± 23.8%, p<0.01] but LAMV/LVEDV remained normal. Isometric exercise resulted in no significant change in hemodynamic parameters.Cardiac rate increased less than 18.7% [from 90.9 ± 20.0 to 107.5 ± 17.9 beats/min] and Qs did not rise significantly. LVESV increased with no EDV change resulting in a fall in EF and VCF. We conclude that in Thal: (1) Surprisingly good ventricular function was maintained despite duration and severity of disease; (2) LV volume changes resulted from the anemic high output state; (3) although normal, LVEF was slightly but significantly reduced; (4) isometric exercise with marked fall in EF and VCF suggested poor myocardial reserve.

HAEMODYNAMIC RESPONSES TO ISOFLURANE ANAESTHESIA AND HYPOVOLAEMIA IN THE DOG, AND THEIR MODIFICATION BY PROPRANOLOL

In six dogs chronically implanted with flow and pressure transducers, equipotent inspired concentrations of halothane and isoflurane were determined as the minimum inspried concentration of each agent which would abolish an individual dog's response to paw clamping. In equipotent concentration, isoflurane (1.2%, SD 0.2%) caused less myocardial depression than halothane (1.0%, SD 0.1%). Dose-response studies were possible up to a mean inspired isoflurane concentration of 3.0%, both before and after propranolol 0.3 mg kg-1, i.v. After propranolol, sensitive indices of myocardial contractility were depressed at all concentrations of isoflurane, indicating a moderate degree of beta-receptor activation by isoflurane. The haemodynamic response to hypovolaemia during isoflurane anaesthesia was not modified by propranolol.

MYOCARDIAL STIMULATION BY PANCURONIUM BROMIDE

The effect of pancuronium bromide on the canine myocardium was studied by observing several indices of myocardial contractility during i.v. and intracoronary infusion of the drug in an anaesthetized, open-chested dog preparation. Pancuronium produced tachycardia when given for 2 min by i.v. and intracoronary infusion with the heart intact. Following denervation and pacing of the heart the intracoronary infusion of the drug produced increases in maximum acceleration of blood at the aortic root, peak aortic blood flow, maximum dP/dt and (maximum dP/dt)/TP. These changes occurred about 30 s after starting the infusion and returned to control values 5 min after stopping the infusion.

The influence of alterations in the cardiac loading conditions on indices of myocardial contractility in the anaesthetized dog.

SUMMARY1. An online analogue computer was used to measure myocardial contractility as the ratio dP/dt/IIT where dP/dt is maximum rate of change of left ventricular pressure and IIT is integrated isometric tension.2. In the open thorax anaesthetized dog, max (dP/dt) and dP/dt/IIT were compared during alterations in preload, by partial vena caval occlusion, and changes in after‐load obtained by acetylcholine injections and by partial occlusion of the descending thoracic aorta.3. A fall in preload lowered max (dP/dt) but did not alter dP/dt/IIT A rise and fall in afterload produced respectively an increase and decrease in max (dP/dt) but dp/dt/IIT was unaltered.4. From expanded time base recordings, the time from the start of aortic flow (EM flowmeter) to max (dP/dt) was measured to indicate the relationship between valve opening and rnax (dP/dt). At low preload or elevated afterload the aortic valve opened well after max (dP/dt) had been reached. When the afterload fell, max (dP/dt) occurred after the opening of the aortic valve.5. Positive inotropic stimulation following intravenous isoprenaline caused a marked elevation in dP/dt/IIT. However, the rise in max (dP/dt) was attenuated in comparison to dP/dt/IIT by a marked fall in afterload and thus early opening of the aortic valve.6. It is concluded that max (dP/dt) is very sensitive to alterations in preload or afterload but the index——‐dP/dt/IIT is normalized so that changes in end diastolic fibre length do not alter this index. When the afterload falls max (dP/dt) is no longer determined in the isovolumic phase of contraction so that magnitude of rnax (dP/dt) is reduced. However, it is an empirical finding that IIT also falls so that the ratio is unaltered. dP/dt/IIT is a useful index of myocardial contractility that is insensitive to changes in preload or afterload.

Effects of dibutyryl cyclic-AMP on cardiac output and myocardial contractility in dogs.

Dibutyryl cyclic-AMP was administered to a group of anesthetized dogs at the doses of 5, 10, 20 and 40 mg/kg, and changes in stroke volume, cardiac output and myocardial contractility were observed. Also, effects of this substance on contractile performance of isolated cardiac muscle were investigated in another group of dogs. Results were as follows: 1) Dibutyryl cyclic-AMP increased heart rate, stroke volume and cardiac output in a dose-related manner in the range from 5 to 40 mg/kg. 2) As indices of myocardial contractility, Vmax and maximum dF/dt were examined. These also showed a dose-dependent increase in response to dibutyryl cyclic-AMP. In isolated dog hearts, dibutyryl cyclic-AMP raised the maximum velocity of shortening (V'max) dose-dependently. 3) Total peripheral resistance declined in a dose-related way. On the other hand, mean arterial pressure and CVP dropped slightly without showing dose-dependence. These results show that dibutyryl cyclic-AMP produces positive inotropic and chronotropic effects and cause dilatation of the peripheral vessels in dose-dependent manners.

Changes in Hemodynamics and Bradykinin Concentration in Coronary Sinus Blood in Experimental Coronary Artery Occlusion

The following parameters were studied before and after acute occlusion of the anterior descending branch of the left coronary artery in 17 dogs: bradykinin (BK) in the coronary sinus blood, heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), left ventricular max dp/dt (LV max dp/dt), and an index of myocardial contractility (LV max dp/dt/IP). BK levels increased, reaching a maximum of 30 +/- 13 ng/ml 2 min after coronary ligation, accompanied by a significant elevation of LVEDP, and lowering of the myocardial contractility index. HR and LV max dp/dt showed no significant changes. A positive correlation obtained between the level of BK and LVEDP, as well as a negative correlation between the level of BK and of both LVSP and myocardial contractility index. Pretreatment with aprotinine (Trasylol), an inhibitor of kinin forming enzyme, prevented the increase in both BK and LVEDP after coronary artery ligation and caused an elevation of myocardial contractility index. These results suggest that BK formed within ischemic myocardium exerts a negative inotropic action on the heart.