Background: Coronary artery disease is a major cause of death in the world. In Yemen acute myocardial infarction (AMI) has increased sharply in recent years due to change in lifestyle of Yemenis. Intensive care units are now available in the big cities. There is no report available to show the pattern of the acute myocardial infarction management including thrombolytic therapy in Yemen. Therefore, we conducted a multicentre study in Sana'a City to determine the in-hospital management of AMI patients, in-hospital morbidity and mortality and the feasibility of establishing a nation-wide and long duration registry in Yemen. Methods: A prospective study enrolled all patients who have been diagnosed as AMI and admitted to the intensive care units in three general hospitals in Sana'a City during the month of May 2000. A specialist filled the data collection form for each patient. Results: 44 patients were admitted with diagnosis of AMI. 86.4% (38 patients) were male and 13.6% (6 patients) were female. All of the patients were Yemenis with a mean age of 51 (-55 years). Compared to the other risk factors current smoking was high at 50% across all age group. History of previous AMI, diabetes, and hypertension, was 6.8%, 6.8% and 18.2% respectively. Two patients (4.5%) gave a history of hypercholesterolemia. Thrombolytic therapy was given to 16 patients (36.4%). These patients presented to hospital within 12 hours from the onset of the symptoms and had no contraindications to thrombolytic therapy. Cardiogenic shock occurred in 10 patients (22.7%), heart failure in 4 patients (9.1%), recurrent ischemia in 4 patients (9.1%) and re-infarction in one patient (2.3%). No stroke or major bleeding was recorded and the total In-hospital mortality rate was 9.1 Prescribing medications at discharge among survivors was 90.5% for aspirin, 72.1% for nitrates, 67.4% for ACE inhibitors, 37.2% for beta-blockers, 11.6% for diuretics, 4.7% for calcium channel blockers and 0% for lipid lowering drugs. Conclusion: The rates of diabetes, smoking, hypercholesterolemia and hypertension were high among our patients being 52.3%, 50%, 22.72% and 18.2% respectively. The use of thrombolytic therapy was not appropriate and need to be improved. The rate of use aspirin and nitrates were adequate while that of b-blockers, ACE inhibitors and lipid lowering drugs need improvement.

In this study, ejection fraction% (EF%) and myocardial performance index (MPI) were recorded in 67 survivors at early, intermediate and late phase of acute myocardial infarction (AMI) .EF% was echocardiographically obtained by the Simpson's method; MPI was calculated using Tissue Doppler Echocardiography (TDE) derived from isovolumetric contraction time (ICT); isovolumetric relaxation time (IRT) and ejection time (ET). Results were compared with those obtained in 70 controls matched for age and sex. At hospital discharge (early evaluation), EF% was < 50% with significant increase in MPI in respect to the healthy controls (increase in ICT, significant reduction in ET and IRT was unchanged). Six months later (intermediate evaluation), EF% still resulted in < 50%, MPI was slightly reduced with further increase in ICT and IRT in comparison to the early evaluation, and slight reduction in ET. Finally, one year later (late evaluation), in spite of increase in EF>50%, MPI was still increased, with slight rise in ICT, almost normalization in ET, but more evident increase in IRT. The outcomes of MPI demonstrate that in post-AMI patients, late prevalent diastolic ventricular dysfunction occurs following an early systolic dysfunction. In this study, EF% appears to be less sensitive than MPI in defining late post-AMI left ventricular dysfunction. Finally, TDE seems to be more sensitive than conventional Doppler method in measuring MPI.

This review article summarizes the results of histopathological and clinical imaging studies to assess myocardial necrosis in humans. Different histopathological features of myocardial cell necrosis are reviewed. In addition, the present role of echocardiographic techniques in assessing irreversible myocardial damage is briefly summarized.

Major causes of rupture of chordae tendinea are myocardial infarction, trauma, hypertension, myxomatous degeneration, endocarditis and rheumatic heart disease. We describe an idiopathic rupture of the chordae tendinea of the posterior mitral leaflet in a 67 years old patient who had no evidence of coronary artery disease, rheumatic disease or other etiologies. The defect was repaired with triangular resection and annuloplasty. He had an uneventful postoperative course for 5 months.