Acute coronary syndrome is a lethal condition. Treatment modality and success mostly depend on time yielded since onset of symptoms. It is known for more than 30 years that delay between symptom onset and treatment of less than 60 min are desirable, but pre hospital delays remain unacceptably long worldwide including Bangladesh. A greater understanding of the contributing factors may help to reduce delays. A number of sociodemographic, clinical, social and proximal factors have been associated with pre hospital delay. The total pre hospital delay period consists of two component: time taken by patients to recognize that their symptoms are serious and to contact medical help (decision time) and the time taken from requesting help to admission where emergency coronary care is available (time to hospital delay). Different factors may affect these two components. In hospital delay also known as door-to-treatment, is defined as time from arriving to hospital to initiation of reperfusion therapy. Regardless of how to shorten in hospital delay, if the pre hospital delay is not reduced, then reperfusion therapy cannot achieve the best results. We set out to discover what factors are specifically associated with three components: decision time, home to hospital delay and First Medical Contact (FMC) to revascularization delay. This review may help the National health management system to identify the factors associated with treatment delay in ACS and thus reduces ACS related morbidity and mortality. University Heart Journal Vol. 15, No. 2, Jul 2019; 79-85

Introduction:The basis of pathophysiologic benefit of revascularization is improving the function of viable myocardium 37 . Early coronary re-canalization helps to survive the viable myocardium and improve global LV function and survival 46 . According to the studies in patients with CAD and LV dysfunction, the disease outcome can be improved with surgical revascularization (CABG) or PCI 37 . PCI in patients with preserved LV function and optimal medical therapy doesn't reduce the cardiac death and MI, but it decreases the need for other procedure and the risk of angina. Its effect on LV systolic or diastolic function is not clear 31 . PCI has been used increasingly for revascularization in ischemic heart disease (IHD) patients. In most of the studies, the primary PCI, criterion such as ejection fraction (EF), diastolic function and the wall motion or chamber sizes has been investigated. But result of previous studies in related area, about elective PCI, has shown unequal viewpoints 1,6,13,27,30,32,39,41 . Intervals between MI and PCI, basic left ventricular ejection fraction (LVEF) before PCI and global condition of the patients affect the result of PCI. Angina occurs when there is regional myocardial ischemia caused by inadequate coronary perfusion and is usually but not always induced by A Study of Changes in Various Echocardiographic

not available University Heart Journal Vol. 16, No. 1, Jan 2020; 11-15

Ventricular septal rupture (VSR) after acute myocardial infarction with the consequence of hemodynamic unstability is a rare complication and it's an medical emergency. Mortality of these group patients is higher than 90% to 95% without a rapid diagnosis and correction by surgical intervention.Spontaneous closure of VSR is extremely rare. We report the case of a patient with acute myocardial infarction with ventricular septal rupture (VSR) with cardiogenic shock that was diagnosed in our modern coronary care unit by the bed side portable echocardiographic machine (vivid).The incidence of ventricular septal rupture (VSR) after acute myocardial infarction is extremely rare in this reperfusion era.This condition is associated with a high mortality rate, even after the cardiac surgery . Our case emphasizes the risk factors and evolution of this condition.A 36 years old young hypertensive young man was admitted on 8 th August,2014 through the emergency department of university cardiac centre for central chest pain ,dyspnea, nausea and bilateral shoulder pain for the last last 7-8 days. He consulted with his family physician for the same complaints and later he was referred to get admission in our hospital. The patient's condition was detoriating gradually. Physical examination revealed a regular pulse of 110 beats/min. The blood pressure was 100/70 mmHg and there was a systolic murmur best heard at the apex, radiating to the axilla. . Pulmonary rales were present and there was no peripheral edema, hepatomegaly and raised JVP.The 12-lead electrocardiogram Figure 1) showed sinus rhythm at 125 beats/ min, low voltage QRS complex voltage in the limb leads, q waves in II,III, AvF and a 4 mm ST elevation in the anterior leads (V 2-4 ).Serum troponin T level at admission was 1.75 ng/ml, CK-MB 28 , Serun creatinine 1.25, Serum electrolytes are within normal limit.He was managed as a case of acute antero-septal MI with old inferior MI and on the following day after his admission he developed cardiogenic shock , examination reveals pulse was 115 beats/min and blood pressure was 80/40 mm of Hg.Then we put the patient under ionotrophic support ,transthoracic echocardiography was done and (figure 2,3 & 4) revealed a small rupture of the apical ventricular septum (figure 2) causing a VSR with left-to-right shunt (figure 3) and Doppler study showed the pressure gradient

not available University Heart Journal Vol. 16, No. 1, Jan 2020; 40-42