[Primary dilated cardiomyopathy].
Recent advances in etiopathogenesis and natural history of idiopathic dilated cardiomyopathy are presented. The clinical and instrumental diagnosis and therapy are also reported.
Biomedical subjects
Publications and source records attributed to L M Profenna.
Recent advances in etiopathogenesis and natural history of idiopathic dilated cardiomyopathy are presented. The clinical and instrumental diagnosis and therapy are also reported.
One hundred and twenty-two patients suffering from slight or moderate essential arterial hypertension with a previous history of myocardial infarction were selected for inclusion in this study. Patients were divided into two groups of 61 according to the type of anti-hypertensive therapy received. Patients in group 1 received nifedipine (30 mg p.d.), while patients in group 2 were treated using other anti-hypertensive therapy (diuretics, alpha-methyldopa, clonidine, indapamide). At the end of the follow-up period, which lasted 5 years, a statistically significant improvement in the following factors was observed in group 1 in comparison to the control group: (a) an improved response of both SBP (p less than 0.001) and DBP (p less than 0.001) levels to anti-hypertensive therapy; (b) a more significant diminution in the thickness of the interventricular septum (p less than 0.001) and the posterior wall of the left ventricle (p less than 0.001) assessed using ultrasonography; (c) a reduced number of cases of post-infarction angina (p less than 0.05); (d) fewer cases of recurrent infarction (p less than 0.05); (e) fewer deaths as a result of re-infarction (p less than 0.01). These results confirm that the vascular and cardioprotective effects of nifedipine give a good long-term outcome in hypertensive patients with a previous history of myocardial infarction.
One hundred and twenty-two patients suffering from slight or moderate essential arterial hypertension with a previous history of myocardial infarction were selected for inclusion in this study. Patients were divided into two groups of 61 according to the type of anti-hypertensive therapy received. Patients in Group 1 received nifedipine (30 mg p.d.), while patients in Group 2 were treated using other anti-hypertensive therapy (diuretics, alpha-methyldopa, clonidine, indapamide). At the end of the follow-up period, which lasted 5 years, a statistically significant improvement in the following factors was observed in Group 1 in comparison to the control group: (a) an improved response of both SBP (p less than 0.001) and DBP (p less than 0.001) levels to anti-hypertensive therapy; (b) a more significant diminution in the thickness of the interventricular septum (p less than 0.001) and the posterior wall of the left ventricle (p less than 0.001) assessed using ultrasonography; (c) a reduced number of cases of post-infarction angina (p less than 0.05); (d) fewer cases of recurrent infarction (p less than 0.05); (e) fewer deaths as a result of re-infarction (p less than 0.01). These results confirm that the vascular and cardioprotective effects of nifedipine give a good long-term outcome in hypertensive patients with a previous history of myocardial infarction.