[Estimation of pulmonary capillary mean pressure using TM-mode echocardiography]. / Die Abschätzung des pulmonalkapillären Mitteldruckes mit Hilfe der TM-mode-Echokardiographie.

The feasibility of estimating the mean pulmonary capillary pressure by simultaneous noninvasive recording of the ECG, the aortic and mitral valve echocardiogram was tested in 50 patients with miscellaneous heart lesions. The Q-MVC-/AVC-E ratio was measured from the onset of the QRS-complex in the ECG, the closure point of the aortic valve, the early diastolic opening of the anterior mitral valve (E-point) and the systolic closure of the mitral valve leaflets on the echocardiogram (C-point). A linear correlation exists between the mean pulmonary artery wedge pressure and the Q-MVC-/AVC-E ratio (n = 50, r = 0.75, p less than 0.001). The echocardiographic derivate index (Q-MVC-/AVC-E) is useful in assessing an elevated left ventricular filling pressure, but the individual data revealed variation in the predicted relation between Q-MVC-/AVC-E and left ventricular end-diastolic pressure. The Q-MVC-/AVC-E ratio is not a useful parameter in predicting left ventricular end-diastolic pressure in patients suffering from a left ventricular aneurysm or an acute transmural myocardial infarction with extensive regional abnormal wall motion. Many criteria such as mitral valve disease, atrial fibrillation, atrioventricular block and left bundle-branch block suggest that the Q-MVC-/AVC-E ratio is of limited clinical value. The left atrial emptying index was measured by using the amplitude of the posterior aortic wall motion occurring in the first third of the passive emptying period.(ABSTRACT TRUNCATED AT 250 WORDS)

Ineffectiveness of methylprednisolone to reduce infarct size in experimental coronary occlusion.

Two medium-sized branches of the left coronary artery were prepared in each of 10 anesthetized open chest dogs for later occlusion. The first artery was occluded during 90 minutes and reperfused thereafter. This occlusion produced the control infarct. Methylprednisolone (50 mg/kg i.v.) was injected and the second artery was occluded also for 90 minutes and reperfused thereafter. Both infarcts were made visible by staining left ventricular rings with p-nitrobluetetrazolium. Infarct size was compared with the size of the perfusion area, which we obtained from the postmortem angiogram. Both infarcts were equal in size and comprised 50% of the area of perfusion of the occluded artery. Methylprednisolone in a single high dose given prophylactically did not influence infarct size nor any of the measured parameters.

The effect of beta-adrenergic blockade on infarct size following experimental coronary occlusion.

The effect of Pindolol on myocardial infarct size was studied in 10 open chest dogs. In each animal a sequential occlusion and reperfusion of 2 medium-sized branches of the left coronary artery was performed in the same heart. After occlusion and reperfusion of the control artery the initial dose of Pindolol (0.25 mg/kg body weight) was administered. Thereafter the test artery was occluded, followed by a maintenance dose of Pindolol (0.3 mg/kg body weight). The drug caused a significant decrease in LVP and LV-dp/dt but no change in heart rate. MVO2 also decreased significantly. Regional myocardial blood flow was measured with the tracer microsphere method. Collateral flow in the perfusion area of the control artery was 11.2 +/- 5.9% and in the area of the test artery 10.0 +/- 4.4% of normal. No change in the endo/epi ratio as a result of treatment was observed. The area of infarction (p-nitroblue tetrazolium-reaction) was divided by the area of perfusion (angiography). Infarct size, expressed as the percentage of the perfusion area, was 48.2 +/- 22.2% in the region of the control artery and 43.0 +/- 23.9% in the region of the test artery. The difference was statistically not significant.

The influence of reperfusin on infarct size after experimental coronary artery occlusion.

Reperfusion following various intervals of coronary occlusion has produced conflicting results: increase in infarct size, especially with hemorrhage into the tissue, was reported as well as salvage of ischemic myocardium. To examine the problem and for the validation of our own method for infarct size measurement, which depends to a certain degree on reperfusion, we occluded two coronary arteries of the same heart in each of 12 open-chest dogs. One artery was reperfused, the other not. Comparable conditions for both occlusions were warranted by selection of small-to-medium sized arteries of equal size and by maintaining of constant MVO2. Reperfused and non-reperfused myocardium did not differ with regard to infarct size, neither after a three-hour nor after a six-hour occlusion. Reperfusion always led to hemorrhagic infarction when performed after six-hour occlusion, while nonreperfused infarctions showed no hemorrhage. Hemorrhage infarcts were not larger as compared to the non-hemorrhagic infarct in the same heart.

Experimental occlusion of two small coronary arteries in the same heart. A new validation method for infarct size manipulation.

A method for the evaluation of interventions aimed at manipulation of infarct size is described. This method has 2 advantages over other methods: 1. Two small-to-medium sized coronary branches of the same heart are occluded and reperfused in sequence. Thereby a "control-infarct" can be compared with a "test-infarct", both within the same heart. 2. The amount of infarcted tissue in both areas is quantitated by using the p-NBT method. A condition of the method is that the areas of perfusion of both arteries are equal. Infarct size is always expressed as a percentage of the perfusion area of the occluded artery. Validation experiments with simultaneous occlusion and reperfusion of both arteries resulted in infarcts of equal size. Validation experiments with regard to the p-NBT method showed that reperfusion accelerates the washout of dehydrogenases from infarcted tissue which allows early and precise diagnosis of infarcts after relatively short occlusion- and reperfusion periods.