ANP concentrations during interchanging DDD-VVI pacing modes in patients with retrograde ventriculoatrial conduction.

The main reason for the pacemaker syndrome during VVI pacing is the existence of ventriculoatrial conduction (V-AC). Twenty-five patients with a permanent DDD pacemaker and ventriculoatrial conduction were included in the study. IN those patients the hemodynamic changes were evaluated in relation to ANP plasma concentration changes during different modes of pacing. After a resting period of 30 minutes in the supine position ANP plasma concentration and blood pressure were evaluated: a) under DDD atrioventricular pacing at 90/min and for 30 minutes and b) under VVI pacing at 90/min and for 30 minutes. A decrease of systolic blood pressure by 12.77% (P < 0.0001) and diastolic blood pressure by 10.50% (P < 0.0001) was noticed during VVI pacing. ANP was increased during VVI pacing by 215.95% (P < 0.0001). It was observed that the acute transition from DDD to VVI pacing leads to a 3-fold increase in the levels of plasma ANP; this may be partially responsible for the pathogenesis of the haemodynamic changes during VVI pacing mediated through the direct hypotensive effect in addition to the coincidence of atrial and ventricular contraction. This study also proves the role of the increased systolic stress of atrial myocardium for the increased ANP secretion.

Increased lung uptake during myocardial scintigraphy improves the detection and localization of coronary artery disease.

Increased lung uptake during exercise thallium 201 scanning denotes severe ventricular hypofunction. To assess whether there is any relationship between this finding and the stenosis of a single coronary artery, the authors studied 140 patients (age 57.5 +/- 12 years) with both exercise thallium and coronary angiography within three months. A planar view was acquired for two hundred forty seconds immediately postexercise and prior to the single photon emission computed tomography acquisition. Two identical regions of interest outlining the left ventricle and the right lung in the planar view were used for calculation of the lung uptake, expressed as a lung-to-heart counts ratio. The patients were divided into four angiographic groups: (I) lesions at the left anterior descending (LAD), n = 35; (II) stenosis at the circumflex (CRX), n = 35; (III) stenosis at the right coronary artery (RCA), n = 35; and (IV) another group of 35 normal subjects serving as controls. No patient had a previous myocardial infraction (MI) or any cardiac operation. Patients in groups I (0.53 +/- 0.094) and II (0.44 +/- 0.072) had higher lung uptake than those in groups III (0.43 +/- 0.061) or IV (0.42 +/- 0.050). There was no difference between groups III and IV, or II and IV, but the difference between I and IV was of statistical significance (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of Q with non-Q myocardial infarction using signal averaged ECG.

Forty consecutive patients (pts) with acute myocardial infarction (MI) who survived to be discharged from the hospital were studied with high gain signal averaged electrocardiography (SAECG). 28% of the pts with non-Q MI had an abnormal SAECG as compared to 15% in the Q MI group. It was also found that SAECG showed a significantly longer filtering QRS duration in the non-Q MI group. The results above were considered as indicative of more delayed activation in pts with non-Q MI providing probably a substrate for more frequent reentrant arrhythmias.

Mechanographic assessment of disopyramide in postinfarction patients.

The inotropic effect of a per os single dose of 200 mg disopyramide phosphate was studied in 25 patients during the second week after acute myocardial infarction with no signs of heart failure. Systolic time intervals and the indices derived from the uncalibrated differentiated carotidogram and apexcardiogram were used to assess changes in cardiac performance. The results were as follows: a) Reduction by 3.2% of the haemodynamic ratio LVET/PEP. b) Reduction by 20.1% of the maximal relative upstroke velocity in the differentiated carotidogram (B/S2) p less than 0.05). c) Decrease by 13.1% of the ratio, total amplitude/dicrotic deflection (T/S2) in the same tracing (p less than 0.05). d) Decrease by 2.8% of the ratio, early systolic wave/early diastolic complex wave (b/ef) in the differentiated apexcardiogram. e) Increase by 3.2% of the ratio early diastolic complex total amplitude (ef/ZN) in the previous tracing. The above changes were indicative of a slight negative inotropic effect of the drug.