Transient Myocardial Dysfunction Research Articles

Right Ventricular Infarction

Right ventricular infarction complicates up to half of inferior left ventricular infarctions. The term represents a spectrum of disease from mild, asymptomatic right ventricular dysfunction to cardiogenic shock, and it includes transient ischemic myocardial dysfunction as well as myocardial necrosis. Right ventricular infarction is associated with considerable morbidity and mortality, and its presence defines a high-risk subgroup of patients with inferior left ventricular infarction. Diagnosis of this condition requires a high degree of suspicion based on clinical findings and the early recording of the electrocardiogram through right precordial leads, as well as elevated right-sided filling pressures out of proportion to left-sided filling pressures. The proper management of right ventricular infarction requires sustaining adequate right ventricular preload with volume loading and maintenance of atrioventricular synchrony, reduction of right ventricular afterload (particularly when left ventricular dysfunction is present), and inotropic support of the right ventricle. Early reperfusion with fibrinolytic therapy or direct angioplasty is also warranted. Survivors of right ventricular infarction generally have a restoration of normal right ventricular function with resolution of hemodynamic abnormalities.

Endocardial Pacing in Infants and Children 15 Kg or Less in Weight: Medium‐term Follow‐Up

Twenty-four children 15 kg or less in weight (range 2.8-15 kg) underwent implantation of a permanent pacemaker using the transvenous technique of lead placement. During a follow-up period of 2 months to 6 years 1 month (median 3 years 6 months) eight children suffered complications, six of which necessitated reoperation. These included: lead fracture in two, infection in two, transient myocardial dysfunction in one, generator migration in one, premature battery depletion in one, and threshold rise in one. A loop of redundant ventricular lead positioned in the atrium at the time of implant is successfully unravelling in all children. One child died during the follow-up period of a pneumonia unrelated to her pacemaker. The other children are growing and developing normally and the cosmetic appearance has proved acceptable in all cases.

Can exercise-induced regional contractile dysfunction be prevented by selective bradycardic agents?

Propranolol (0.5 mg X kg-1 X 5 min-1), alinidine (1 mg X kg-1 X 5 min-1) and the benzazepinon UL-FS 49 (0.5 mg X kg-1 X 5 min-1) were investigated in a canine model of exercise-induced transient myocardial dysfunction, mimicking exercise-induced functional impairment during angina pectoris in man. Each drug was infused intravenously, after two control treadmill exercise runs had shown comparable, ultrasonically assessed regional contractile dysfunction in an area supplied by a partly stenosed branch of the left coronary artery. All three drugs abolished exercise-induced regional contractile dysfunction. Propranolol and alinidine comparably decreased heart rate and positive dp/dtmax during exercise. UL-FS 49 showed a marked negative chronotropic effect without affecting positive dp/dtmax. Thus, prevention of exercise-induced regional contractile dysfunction has been shown for the first time using a selective bradycardic agent.

A model of transient myocardial dysfunction in conscious dogs: Regional shortening in the presence of impaired coronary flow reserve and treadmill exercise

An experimental model of treadmill exercise-induced regional myocardial dysfunction was developed in conscious dogs to mimic exertional angina pectoris in man. Twenty mongrel dogs, trained to run on a treadmill, were chronically instrumented with a miniature pressure transducer in the left ventricle and a hydraulic occluder placed around the circumflex branch of the left coronary artery. Two pairs of piezoelectric crystals for sonomicrometry were implanted subendocardially to measure regional myocardial function. Experiments were started 1 week after surgery. In the first group of ten dogs exercise with constant work load of 10 km/hr and 10% elevation during partial left coronary artery stenosis, induced by external filling of the occluder, produced comparable episodes of regional dysfunction in the left coronary artery area during five subsequent treadmill runs and recovery of function after each run. The second group of ten dogs, exercised with left coronary artery stenosis and increasing working load, exhibited minimal regional dysfunction in the left coronary artery area while running at 6 km/hr and 6% elevation, but maximal regional dysfunction during peak exercise (10 km/hr and 10% elevation). This load dependency and recovery of function after the runs was demonstrated during five identical consecutive exercise cycles. This model, in contrast to those using ameroid constrictors, enables various drugs to be tested in a single instrumented dog over a period of several weeks.

Transient myocardial dysfunction during pharmacologic vasodilation as an index of reduced coronary reserve: A coronary hemodynamic and echocardiographic study

Regional coronary flow reserve and regional myocardial contractility were evaluated in 29 patients after maximal pharmacologic coronary vasodilation (intravenous dipyridamole, 0.56 mg/kg body weight, administered over 4 minutes). Nineteen patients had a severe (80 to 99%) proximal and isolated stenosis of the left anterior descending coronary artery and 10 patients had normal coronary arteries; all had normal ventricular function under rest conditions. Myocardial contractility was assessed by means of continuous two-dimensional echocardiographic monitoring; coronary reserve was evaluated by coronary sinus thermodilution. After dipyridamole infusion, 9 of the 19 patients with left anterior descending artery stenosis had transient myocardial asynergy involving the septum or apex, or both (Group IA), whereas 10 patients showed no asynergy (Group IB). No impairment of contractility was observed in the 10 patients with normal coronary arteries (Group II). Coronary blood flow was measured under basal conditions and up to 10 minutes after the end of dipyridamole infusion. In patients in Group II, dipyridamole induced an increase in great cardiac vein flow of 167 +/- 68% (mean +/- SD). The 10 patients in Group IB showed a response comparable with that of the control group (Group II) (136 +/- 45% increase in great cardiac vein flow; NS versus Group II), whereas the 9 patients in Group IA had an increase of 46 +/- 30% (p less than 0.01 versus both Group IB and Group II). No significant difference was found in the angiographic severity of the stenosis expressed in terms of minimal cross-sectional area (Group IA = 0.30 +/- 0.13 mm2, Group IB = 0.34 +/- 0.18 mm2; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Transient Drug-Induced Myocardial Dysfunction is Not Ameliorated by PGI2 in Dogs

Prostacyclin (PGI2), a potent vasodilatory substance that effectively inhibits platelet aggregation is under clinical investigation for the treatment of angina pectoris. We studied the effects of PGI2 on transient drug-induced myocardial dysfunction in anesthetized, thoracotomized dogs. Regional myocardial function was assessed using two pairs of piezoelectric transducers and a multidimensional measuring gauge; one pair was implanted in the distribution area of the left circumflex branch (LCX) and the other in the distribution area of the descending branch (LAD) of the left coronary artery. After intravenous injection of isoproterenol (ISO), which led to an increase in systolic shortening in the LCX and LAD areas, a critical stenosis was performed on the LCX and maintained at this level. Intravenous ISO injection now induced regional dysfunction in the LCX-dependent segment with the occurrence of systolic bulging. Infusion of PGI2 at a dosage of 100 ng/kg/min caused a decrease in arterial blood pressure and an increase in heart rate, but had no effect on regional myocardial function. ISO-induced myocardial dysfunction in the critically stenosed LCX segment, which was observed before PGI2 administration, was not ameliorated, but rather aggravated, by PGI2. It may be concluded that PGI2 does not improve normal or ISO-stimulated myocardial function in pressure-dependent perfused areas of the heart.

A canine model of transient myocardial dysfunction regional shortening in the presence of critical stenosis and cardiac stimulation

An experimental model of exercise-induced angina pectoris was developed in anesthetized dogs. Two i.v. bolus injections of isoproterenol (ISO, 0.25 μg kg ; time interval: 10 min) were administered, followed by constriction of the circumflex coronary artery (LCX; critical stenosis). Further i.v. bolus injections of ISO were administered before and after i.v. infusion of 0.9% NaCl (control infusion). Stenosis of the LCX did not modify regional function at rest as assessed with ultrasonic crystals implanted subendocardially both in the distribution areas of the circumlfex coronary artery and of the left anterior descending coronary artery (LAD). In the presence of critical stenosis, ISO induced a reproducible, transient decrease in systolic shortening and percent systolic shortening in the area supplied by the LCX and a marked increase in systolic shortening and percent systolic shortening in the area supplied by the LAD. During a 60-min observation period following control infusion, no further substantial changes in regional dimensions were observed. The ISO-induced hemodynamic changes were reproducible during this period. The experimental model of exercise-induced angina pectoris presented in this study can be assumed to provide a reliable basis for evaluating the efficacy of various therapeutical interventions.

Coronary hemodynamics during percutaneous transluminal coronary angioplasty

The hemodynamic consequences of multiple transient occlusions (9.8 ± 3.7 seconds) of the left anterior descending coronary artery were assessed in 15 conscious patients during percutaneous transluminal coronary angioplasty. Thermodilution coronary venous blood flow, measured in the great cardiac vein, decreased from control values of 75.9 ± 24 ml/min to 50.9 ± 21.9 with coronary occlusion (probability [p] < 0.00001) and increased to 101.6 ± 34.3 after release of occlusion (p < 0.00001). Changes in coronary sinus blood flow, measured simultaneously, reflected the alterations in the great cardiac vein. Restoration of postocclusion blood flow to control values occurred in 18.2 ± 6.7 seconds, and is compatible with reactive hyperemia rather than sustained improvement in resting coronary blood flow. Flow repayment during reactive hyperemia exceeded flow debt incurred during coronary occlusion by 288.4 ± 106 percent (p < 0.05). The increase in reactive hyperemic flow after initial coronary occlusion (24.2 ± 15.7 ml/min) was less than that after final occlusion (42.2 ± 10.1, p < 0.05). This suggests an initial limitation of reactive hyperemia by persistent coronary stenosis. In all patients, reactive hyperemia accentuated the trans-stenotic coronary ostial to distal coronary arterial pressure gradient. Compared with a control value of 53.5 ± 7.7 percent, the great cardiac vein oxygen saturation transiently decreased to 49.3 ± 7.0 percent (p < 0.001) on release of the occlusion and then increased to 62.5 ± 5.2 percent (p < 0.001) during reactive hyperemia. A small reduction in aortic pressure from 96.4 ± 10.2 mm Hg to 89.9 ± 10.9 mm Hg(p < 0.00001) was observed during occlusion. A reduction in first derivative of left ventricular pressure (dP/dt) during coronary occlusion, in three patients in whom it was measured, suggests that the decrease in systemic pressure is due to transient ischemic myocardial dysfunction rather than to peripheral arteriolar vasodilation. These observations are relevant to the performance of coronary angioplasty, and to the understanding of the physiology of transient coronary occlusion in conscious patients.

Contractile damage from reperfusion after transient ischemia in the dog

The patterns of regional contractile function were examined with ultrasonic crystals in "open-chest" anesthetized dogs. In normal myocardium, the base-line end-diastolic segment length (EDL) was 1.63 +/- 0.12 cm. and the mean systolic length (MSL) was 1.47 +/- 0.17 cm. Mean velocity of shortening over the first one third of systole (V1/3) was 15.9 +/- 2.3 mm. per second. Coronary occlusion induced regional ischemia with segmental dyskinesia (MSL = 1.84 +/- 0.12 cm). Reperfusion after 5 or 10 minutes of occlusion induced rapid recovery of contractile function that was independent of catecholamine release, as demonstrated in animals pretreated with 6-OH dopamine. After initial recovery, however, contractile function deteriorated. There were an increase in EDL (from 1.73 +/- 0.11 to 1.78 +/- 0.11; p less than 0.001) and the appearance of early systolic dyskinesia. V1/3 diminished from 5.6 +/- 4.6 to -6.6 +/- 2.5 mm. per second (p less than 0.005). Thus reperfusion damage, defined as late deterioration after recovery from brief periods of ischemia, may be partly distinct from ischemic damage per se. It is possible that the deterioration of myocardial function which accompanies reperfusion of previously ischemic myocardium may be a contributing factor in the transient myocardial dysfunction that is occasionally seen following cardiopulmonary bypass.