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Several experimental studies are conducted to explain the genetic determinants that are associated with the Lp(a) lipoprotein level and the coronary disease in patients. The Lp(a) lipoprotein is shown to exhibit a significant role in the onset of the coronary disease.

Byline: Massimo Villella, Alessandro Villella, Simona Barlera, Maria Grazia Franzosi, Aldo P. Maggioni Abstract: Background The aim of this study was to evaluate the prognostic significance of the pressure-rate product (PRP) obtained during exercise stress testing and of its change from rest to maximal exercise (dPRP) in a population of survivors of acute myocardial infarction treated with thrombolytic agents. Methods And Results Survivors of acute myocardial infarction (n = 6251) from the GISSI-2 database, who underwent a maximal symptom-limited exercise test with either bicycle ergometer or treadmill, were followed up for 6 months. PRP and dPRP values were dichotomized ([less than or equal to]21,700 and >21,700, [less than or equal to]11,600 and >11,600, respectively) and analyzed in a multivariate Cox model individually and simultaneously with other ergometric variables. Six-month mortality rate was 0.8% in the high PRP group and 2.0% in the low PRP group. Low PRP was an independent predictor of 6-month mortality rate (relative risk [RR] 1.97, 95% confidence interval [CI] 1.24 to 3.13). Patients with low dPRP had mortality rates higher than patients with high dPRP (2.1% vs 0.8%). At the multivariate analysis, low dPRP showed negative predictive value (RR 1.97, 95% CI 1.23 to 3.16). A further multivariate analysis was performed with PRP and dPRP, also adjusting for low work capacity, abnormal systolic blood pressure response to exercise, and symptomatic-induced ischemia. The results showed that low work capacity, low PRP, and symptomatic exercise-induced ischemia were still significantly associated with higher 6-month mortality rate (P = .04, .02, and .05; RR = 1.68, 1.71, and 1.78 respectively). Conclusions PRP is a predictive index to assess prognosis in survivors of acute myocardial infarction treated with thrombolytic agents able to perform an exercise test after acute myocardial infarction, but its usefulness appears to be limited, considering that these patients were at low risk. (Am Heart J 1999;137:443-52.) Author Affiliation: Milan, Italy From Ospedale 'Casa Sollievo della Sofferenza' IRCCS, S Giovanni Rotondo; and Istituto di Ricerche Farmacologiche Mario Negri .sup.*A complete list of the investigators and centers participating in GISSI-2 has been published (Lancet 1990;336:65-71). The Steering Committee consisted of G.A. Feruglio, A. Lotto, F. Rovelli, P. Solinas, L. Tavazzi, and G. Tognoni. The study was endorsed by the Associazione Nazionale Medici Cardiologi Ospedalieri and the Istituto di Ricerche Farmacologiche Mario Negri Article History: Received 30 July 1997; Accepted 17 April 1998 Article Note: (footnote) [star] Reprint requests to: Massimo Villella, MD, GISSI-2 Coordinating Centre, Via Eritrea, 62-20157 Milano, Italy., [star][star] 0002-8703/99/$8.00 + 0 4/1/91121

Treatment with recombinant (genetically engineered) tissue plasminogen activator (t-PA) to break up blood clots may slightly increase the risk of a stroke in heart attack patients. Of 20,768 patients hospitalized for a heart attack, 10,396 were treated with streptokinase, 10,372 were treated with t-PA, 10,361 simultaneously received subcutaneous heparin, and 10,407 did not receive heparin. Ninety-one percent also received aspirin. Streptokinase and t-PA break up blood clots, while heparin and aspirin prevent their formation. Among these patients, 236 (one percent) suffered a stroke in the hospital. Of the patients who had strokes, 74 (36%) had a stroke caused by intracerebral hemorrhaging, 100 (42%) had an ischemic stroke and 62 (26%) had a stroke of unknown cause. Patients treated with t-PA were more likely to have a stroke than those treated with streptokinase. Patients treated with heparin did not have more strokes than those who did not receive heparin.