Post-ejection thickening as a marker of viable myocardium. An echocardiographic study in patients with chronic coronary artery disease.

The study aim was to assess whether post-ejection thickening (PT) is an useful marker of viable myocardium in patients with chronic coronary artery disease. Twenty-three patients with critical coronary stenoses were submitted to dobutamine and dipyridamole stress-echocardiographies and dipyridamole-early-redistribution 201Tl SPECT within 15 days from coronary arteriography. They were selected for the presence of PT in segments that could be optimally studied by M-mode echocardiography and were hypo-akinetic in basal conditions. PT (occurring between end-ejection and mitral valve opening) was found in 58% of dysfunctional, critically perfused regions. Ninety-eight percent of the regions with PT and 6% of those without PT improved during low-dose dobutamine stress-echocardiography. Segments with PT had, respectively, higher and lower SPECT early-redistribution thallium activity than dysfunctional segments without PT and normokinetic regions. Therefore, regions with PT were viable and had a moderate decrease in coronary perfusion. Akinetic segments without PT did not show any inotropic reserve. After revascularization almost all the segments with PT improved. In conclusion, PT is a pattern of myocardial contraction easily detected by M-mode echocardiography in the clinical setting. If the results of this study are further confirmed, PT may become a sign for the recognition of myocardial viability.

Dipyridamole angina: a specific symptom of severe multivessel disease.

BACKGROUND: Several studies have indicated that ischemia induced by dipyridamole is frequently associated with angina or ischemic ST-segment depression and that it occurs mainly in patients with three-vessel disease, those with collateral vessels, or those with both. METHODS: In order to analyze the diagnostic relationships among them, we studied 227 consecutive patients who underwent coronary angiography and dipyridamole-thallium scintigraphy. RESULTS: A perfusion defect was found in 134 patients. Of these, 88 patients (66%) showed no significant ECG modifications or angina; 46 (34%) had a transient ST-segment depression, which was associated with typical angina ('dipyridamole angina') in 12. These 12 patients had three-vessel disease with intercoronary collateral circulation. Among the 134 patients with coronary critical stenoses and a positive thallium-dipyridamole test, collateral vessels were detected in 91 (68%). CONCLUSION: Dipyridamole angina, occurring during a positive dipyridamole-thallium test, is usually a manifestation of severe coronary stenoses with collateral circulation. However, as a diagnostic symptom it is characterized by high specificity but low sensitivity.

Serum theophylline concentrations and pulmonary function tests after administration of two sustained-release formulations containing theophylline in patients affected by chronic obstructive lung disease.

We compared serum theophylline concentrations in patients treated with one of two commercially available theophylline preparations: a sustained-release aminophylline and a sustained-release theophylline. Two comparable groups of 15 out-patients with stable, chronic obstructive lung diseases were studied: one group was given sustained-release aminophylline while the other took sustained-release theophylline. Both drugs were administered orally for 7 days at a daily dose, equivalent to 12 mg/kg in terms of anhydrous theophylline. Serum theophylline concentrations were always significantly lower after treatment with sustained-release aminophylline than after treatment with sustained-release theophylline, which latter frequently caused undesirable side-effects. Moreover, patients receiving sustained-release aminophylline always showed serum theophylline concentrations lower than 10 mcg/ml. Pulmonary function tests were unaffected by the administration of either drug. We conclude that sustained-release theophylline is more effective than sustained-release aminophylline in terms of induced serum theophylline concentrations. However neither drug was suitable for the treatment of patients with chronic obstructive lung disease without other concomitant therapy.

Acute effect of furosemide on renal kallikrein and prostaglandin systems in mild to moderate essential hypertension.

The activity of basal 24-hour urinary kallikrein activity (UKA), prostaglandin E2 (U. PGE2) and thromboxane B2 (U. TxB2) and their relationship to natriuresis (U. Sodium), urinary aldosterone (U. Aldosterone) and plasma renin activity (in supine position: PRA1; in standing position: PRA2) were evaluated in 20 patients with early-moderate hemodynamically defined (first pass and gate blood pool radionuclide angiocardiography) essential hypertension (H) and in 13 age-matched normotensive patients (N). In basal conditions, UKA and PRA2 were significantly reduced (p less than 0.005 and p less than 0.05, respectively) in H compared with N. However, no differences between N and H were found for U. TxB2, U. PGE2, U. Aldosterone, U. Sodium, and PRA1. All parameters were also evaluated both in H and N before and after the administration of furosemide (40 mg i.v.). In H, but not in N, furosemide induced an increase of UKA (p less than 0.05), U. TxB2 (p less than 0.05) and U. Sodium (p less than 0.001). In both H and N furosemide caused a significant rise of PRA1 (p less than 0.001 in H and p less than 0.01 in N) and PRA2 (p less than 0.001 in H and p less than 0.05 in N). In H a significant correlation was found between percent increases of U. Sodium and U. Kallikrein (r = 0.54, p less than 0.01) and between percent differences of PGE2 and TxB2 (r = 0.59, p less than 0.01). It is proposed that reduction of basal UKA may be an early evidence of the first stages of hypertension, i.e., in absence of renal and cardiovascular alteration. The finding is not accompanied by significant changes in urinary excretion of arachidonic acid metabolites and aldosterone. Finally, any relation between UKA values and systemic hemodynamics is lacking.