The heart is a muscular organ enclosed in protective fibrous sac (the pericardium), a fibrous layer is also closely affixed to the heart called the epicardium.

The wall of the heart is composed primarily of cardiac muscle cells, the myocardium.

The inner surface of the cardiac chambers as well as the inner wall of all blood vessels is lined by a thin layer of cells known as endothelium.

Cardiac muscle:

It is specialized muscle cells with amazing resiliency and stamina arranged in layers that are tightly bound together and completely encircle the blood filled function when the walls of the walls of a chamber contract they come together like squeezing fist and exert pressure on the blood they enclose.

Every heart cell contracts with every beat of the heart. The human heart has a limited ability to replace it is muscle cells. Recent experiments suggest that only about 1% of heart muscle cells are replaced per year.

The blood being pumped through the heart chambers does not exchange nutrients metabolic end products with the myocardial cells. They like the cells of all other organs receive their blood supply via arteries that branch from the aorta called coronary arteries [1] .

Coronary circulation:

Coronary anatomy varies greatly from person to person There are many normal

Myocardial infarction or Heart attack: Under group acute coronary syndrome defined as acute myocardial ischemia with evidence of myocardial necrosis of an area of myocardium occurring as a result of critical imbalance between coronary blood supply and myocardial demand.

The Third Universal Definition of myocardial infarction (MI) expert consensus document was published in October 2012 by the global Myocardial Infarction Task Force so:

An myocardial infarction is defined by a typical rise and or fall of cardiac troponin (cTn), With at least one value above the assays upper reference limit (URL) accompanied by at least one of the other feature of ischemia e.g. typical symptoms or ECG [1] [2] .

Type 1: Spontaneous MI

Spontaneous MI due to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD, non-obstructive coronary disease or no CAD.

Type 2: MI secondary to an ischemic imbalance

Myocardial injury with necrosis occurs due to conditions other than CAD that contribute to an imbalance between myocardial oxygen supply and/or demand such as coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachycardia-bradycardia arrhythmias, anemia, respiratory failure, hypotension, and hypertension.

Type 3: MI resulting in death when biomarker values are unavailable

Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurs before blood samples can be obtained, before cardiac troponins biomarkers rise, or when cardiac biomarkers were not collected.

Type 4A: MI related to percutaneous coronary intervention

MI associated with PCI is defined by elevation of cTn values greater than five times the 99th percentile upper normal reference limit (URL) in patients with normal baseline values (<99th percentile URL) or a rise of cTn values by >20% if the baseline troponins are elevated and are stable or falling. In addition one of the following criterion are required: 1) symptoms suggestive of myocardial ischemia; 2) new ischemic ECG changes or new LBBB; 3) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no coronary flow or coronary embolization; or 4) demonstration with imaging of a new loss of viable myocardium or new regional wall motion abnormality.

Type 4B: MI related to stent thrombosis

MI associated with stent thrombosis detected by coronary angiography or autopsy in the presence of myocardial ischemia with a rise and/or fall of troponin biomarkers. One troponin measurement should be above the 99th percentile UR.

Type 4C: MI related to restenosis

MI associated with restenosis defined as ≥50% stenosis or a complex lesion demonstrated at coronary angiography after initial successful stent.

Deployment or dilatation of a coronary artery stenos is with balloon angioplasty. These coronary angiographic changes should be associated with an increase and/or decrease of cTn values > 99th percentile URL and no other significant obstructive CAD.

Type 5: MI related to coronary artery bypass grafting

MI associated with CABG is defined by elevation of cardiac troponins greater than ten times the 99th percentile URL in patients with normal baseline cTn values (<99th percentile URL). In addition, one of the following should be present: new pathological Q waves or new LBBB; or angiographic documented new graft or new native coronary artery occlusion or new loss of viable myocardium or new regional wall motion abnormality as shown by an imaging modality [10] .

Myocardial infarction is defined by pathology as myocardial cell death due to prolonged ischemia. Cell death categorized pathologically as coagulation and/or contraction band necrosis, which usually evolves through oncosis but can result to a lesser degree from apoptosis. Careful analysis of histological sections by an after the onset of myocardial ischemia, cell death is not immediate but takes a finite period to develop (as little as 20 min or less in some animal models). It takes several hours before myocardial necrosis can be identified by macroscopic or microscopic post-mortem examination. Complete necrosis of all myocardial cells at risk requires at least 2 - 4 h or longer depending on the presence of collateral circulation to the ischemic zone persistent or intermittent coronary arterial occlusion the sensitivity of the myocytes to ischemia, pre-conditioning, and/or finally individual demand for myocardial oxygen and nutrients. Myocardial infarctions are usually classified by size: microscopic (focal necrosis), small (10% of the left ventricular [LV] myocardium), moderate (10% - 30% of the LV myocardium) and large (30% of the LV myocardium), and by location. The pathological identification of myocardial necrosis is made without reference to morphological changes in the coronary arterial tree or to the clinical history [3] . The vast majority of MIs are caused by acute coronary artery thrombosis. In most instances disruption of preexisting atherosclerotic plaque serves, as the nidus for thrombus generation, vascular occlusion, and subsequent transmural infarction of the downstream myocardium. In 10% of MIs, however transmural infarction occurs in the absence of occlusive atherosclerotic vascular disease such infarcts are mostly attributable to coronary artery vasospasm or to embolization from mural thrombi [4] .

Myocardial Response to Ischemia: Loss of the myocardial blood supply leads to profound functional, biochemical and morphologic consequences. Within seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in adenosine triphosphate (ATP) and accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes. The functional consequence is a rapid loss of contractility, which occurs within a minute or so of the onset of ischemia. These early changes are potentially reversible. Only severe ischemia lasting at least 20 to 40 minutes causes irreversible damage and myocyte death leading to coagulation necrosis [5] .

The microscopic appearance also undergoes a characteristic sequence of changes and typical features of coagulative necrosis become detectable within 4 to 12 hours of infarction. “Wavyfibers” also can be present at the edges of an infarct; these reflect the stretching and buckling of noncontractile dead fibers. Sublethal ischemia can also induce intracellular myocyte vacuolization; such myocytes are viable but frequently are poorly contractile (see Table 1 and Figure 1).

Irreversible Injury

central yellow-tan softening necrosis; pyknosis of nuclei; myocytehypereosinophilia; marginal contraction band necrosis; beginning neutrophilic infiltrate Coagulation necrosis, with loss of nuclei and striations; interstitial infiltrate of neutrophils Beginning disintegration of dead myofibers, with dying neutrophils; early phagocytosis of dead cells by macrophages at infarct border 01. In a typical MI, the following sequence of events transpires: There is a sudden disruption of an atheromatous plaque-for example, intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring-exposing subendothelial collagen and necrotic plaque contents.

Platelets adhere, aggregate, become activated, and release potent secondary aggregators including thromboxane A₂, adenosine diphosphate, and serotonin.

Vasospasm is stimulated by platelet aggregation and mediator release.

Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of the thrombus. Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel.

While the classic symptoms of a heart attack are chest pain and shortness of breath, the symptoms can be quite varied. The most common symptoms of a heart attack include:

pressure or tightness in the chest, pain in the chest back, jaw and other area of the upper body that lasts more than few minutes or that goes away and come back shortness of breath, sweating, nausea, vomiting, anxiety, cough, dizziness & tachycardia. It is important to note that not all people who have heart attacks experience the same symptoms or the same severity of symptoms. Chest pain is the most commonly reported symptom among both women and men. However, women are more likely than men to have shortness of breath, jaw pain, upper back pain, lightheadedness, nausea & vomiting. In fact some women who have had a heart attack report that their symptoms felt like the symptoms of the flu [6] .

A) Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases. Approximately 90% of myocardial infarctions (MIs) result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary thrombosis and occlusion. Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the pathogenesis of vulnerable plaque formation [7] . A large body of evidence indicates that in numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary tree [8] [9] . Coronary atherosclerosis is especially prominent near branching points of vessels. Culprit lesions that are particularly prone to rupture are atheromascontaining abundant macrophages, a large lipid-rich core surrounded by a thinned fibrous cap [11] (See Table 2).

B) MI can also occur for causes other than atherosclerosis (Nonatherosclerotic) causes of MI include the following:

1) Coronary occlusion secondary to vasculitis; new researches shows that inflammation also plays a role in the evolution of heart attacks. It appears that the coronary artery walls become inflamed over time, further increasing the buildup of fatty plaques.

2) Ventricular hypertrophy (e.g. left ventricular hypertrophy, hypertrophic cardiomyopathy).

3) Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis.

4) Coronary trauma.

5) Primary coronary vasospasm (variant angina); heart attacks may also be caused by coronary artery spasm, where a heart artery is temporarily constricted, using tobacco and illicit drugs, such as cocaine, can cause a life-threatening spasm.

6) Drug use (e.g. cocaine, amphetamines, ephedrine).

7) Arteritis.

8) Coronary anomalies, including aneurysms of coronary arteries.

9) Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism.

10) Factors that decrease oxygen delivery, such as hypoxemia of severe anemia.

11) Aortic dissection, with retrograde involvement of the coronary arteries.

12) Respiratory infections, particularly influenza [12] [13] .

C) In addition, MI can result from hypoxia due to carbon monoxide poisoning or acute pulmonary disorders.

D) Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis. Acute MI is rare in childhood and adolescence. Although adults acquire coronary artery disease from lifelong deposition of atheroma and plaque, which causes coronary artery spasm and thrombosis, children with acute MI usually have either an acute inflammatory condition of the coronary arteries or an anomalous origin of the left coronary artery.

Intrauterine MI also does occur, often in association with coronary artery stenosis [14] .

In 1971, WHO proposed that the diagnosis of myocardial infarction required the presence of at least 2 of the following:

1) Typical symptoms.

2) Typical ECG pattern involving the development of Q waves.

3) An initial rise and subsequent fall in serum or plasma Biomarkers of myocardial necrosis [15] .

1-History and physical Examination: Note that up to 30% of MI are recognized or silent due to Atypical symptoms more common in women, DM, elderly, post Heart transplant because of denervation [16] . *The first step is to determine if the pain is truly cardiac in nature [17] . The assessment of acute chest pain depends on analysis of character of the pain or collapse and it is associated features. If the history of chest pain is strongly consistent with ischemia, it is more important than EKG alone (See Table 3).

2-ECG: ECG is critical if the patient was admitted for chest pain. It is central to confirming the diagnosis but may be difficult to interpret if there is BBB or previous MI. the initial ECG may be normal or normal diagnostic in one third of cases. Repeated or serial ECG are important especially if the diagnosis is uncertain or the or if the patient has recurrent or persistent symptoms.

3-plasma cardiac biomarkers: Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into blood stream. the third universal definition of myocardialinfarction recommends that patients who are suspected on clinical grounds of having ACS should undergo serial sampling for cardiac troponin (cTn). Now, the markers most widely used in detection of myocardial infarction are CK-MB and cTn T and I, as they are more specific for myocardial injury. Troponin T and I have nearly complete tissue specificity myocardial damage [18] .

Other serum cardiac markers:

Until 1980, enzymes AST or SGOT and LDH were used to assess cardiac injury. May be from damaged red blood cells, kidney, liver and lung, usually not performed now except in small centers [3] .

#Other blood test: CBC (polymorphoneuclear leukocytosis), ESR: raised chest X ray: may demonstrate pulmonary edema. Heart size is usually normal. Enlarged cardiac shadow indicates preexisting myocardial damage [2] [3] .

Echocardiography:

May be performed in equivocal cases. Useful for assessing ventricular function and for detecting important complication [2] .

Coronary angiogram:

Allows visualization of narrowing or obstruction on heart vessels.

It is performed in difficult cases or in situation where the intervention to restore blood flow is appropriate .Catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart radio opaque dye is administered through the catheter and a sequence of X ray (fluoroscopy is performed.

Nuclear medicine:

Can be used in stable patient whose symptoms have resolved by the time of evaluation as technetium 99 mtcsestamibi, thallium 201 chloride or rubidium 82 chloride to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress [8] [9] .

Significance

• Negative first testexcludes nothing

• Positive test suggests Ml

• False positive with CHF and renal failure

• Cannot detect re infarction in last week

• Negative first test excludes nothing

• Positive test suggests Ml

• Best test for detecting re infarction

• Lacks specificity

• Negative test at 4 hours excludes Ml

• Positive test is useless

• Continued pain with maximal medical therapy needs angiography

• Normal BNP excludes CHF

• Abnormal test is Nonspecific

• Reversible ischemia is the main thing you are looking for

• Catheterize abnormal

• Normal wall motion excludes Ml

• High troponin with normal wall motion is a false-positive troponin

• All ACS patients need telemetry

Pre-hospital care: oxygen, aspirin, nitrates, and triage to an appropriate medical center (see Figure 2).

Drug treatment: Anti-platelet drugs, anti-anginal drugs, anticoagulants, and in some cases other drugs.

Reperfusion therapy: Fibrinolytics or angiography with percutaneous coronary intervention or coronary artery bypass surgery.

Postdischarge rehabilitation and chronic medical management of coronary artery disease. Choice of drug therapy and choice of reperfusion strategy are discussed elsewhere.

Pre-hospital care: Oxygen, aspirin, nitrates & triage to appropriate medical center. A reliable IV route must be established, oxygen given (typically 2 L by nasal cannula), and continuous single-lead ECG monitoring started. Prehospital interventions by emergency medical personnel including ECG.

Hospital admission: Risk-stratify patient and choose reperfusion strategy. Drug therapy with anti-platelet drugs, anticoagulants and other drugs based on reperfusion strategy. On arrival to the emergency room, the patient’s diagnosis is confirmed. Drug therapy and timing of revascularization depend on the clinical picture and diagnosis. For STEMI, reperfusion strategy can include fibrinolytic therapy or immediate PCI. For patients with NSTEMI, angiography may be done within 24 to 48 h of admission if the patient is clinically stable. If the patient is unstable (e.g. ongoing symptoms, hypotension or sustained arrhythmias), then angiography must be done immediately [19] .

Morphine should be used judiciously (e.g. if nitroglycerin is contraindicated or if the patient has symptoms despite nitroglycerin therapy).

Complicated means that the hospital course was complicated by recurrent angina or infarction, heart failure, or sustained recurrent ventricular arrhythmias. Absence of any of these events is termed uncomplicated.

Drug treatment of acute myocardial infarction

All patients should be given anti platelet drugs, anticoagulants, and if chest pain is present, anti-anginal drugs. The specific drugs used depend on the reperfusion strategy and other factors; their selection and use is discussed in drugs for Acute Coronary Syndrome. Other drugs, such as beta-blockers, ACE inhibitors, and statins, should be initiated during admission.

Patients with acute myocardial infarction should be given the following (unless contraindicated):

• Anti-platelet drugs: Aspirin, clopidogrel, or both (prasugrel or ticagrelor are alternatives to clopidogrel).

• Anticoagulants: A heparin (unfractionated or low molecular weight heparin) or bivalirudin.

• Glycoprotein IIb/IIIa inhibitor for some high risk patients.

• Antianginal therapy usually nitroglycerin.

• Beta-blockers.

• ACE inhibitor.

• Statin.

All patients are given aspirin 160 to 325 mg (not enteric-coated), if not contraindicated, at presentation and 81 mg once/day indefinitely thereafter. Chewing the first dose before swallowing quickens absorption. Aspirin reduces short-term and long-term mortality risk. In patients undergoing PCI, a loading dose of clopidogrel (300 to 600 mg po once), prasugrel (60 mg po once), or ticagrelor (180 mg po once) improves outcomes, particularly when administered 24 h in advance. For urgent PCI, prasugrel and ticagrelor are more rapid in onset and may be preferred. Either a low molecular weight heparin (LMWH), unfractionated heparin, or bivalirudin is given routinely to patients unless contraindicated (e.g. by active bleeding).

Unfractionated heparin is more complicated to use because it requires frequent (q 6 h) dosing adjustments to achieve target activated PTT (aPTT). The LMWHs have better bioavailability, are given by simple weight-based dose without monitoring aPTT and dose titration, and have lower risk of heparin-induced thrombocytopenia. Bivalirudin is recommended for patients with a known or suspected history of heparin-induced thrombocytopenia. Anticoagulants are continued for:

• Duration of PCI in patients undergoing this procedure.

• Duration of hospital stay (in patients on LMWH) or 48 h (in patients on unfractionated heparin) in all other cases.

Consider a glycoprotein IIb/IIIa inhibitor for high-risk patients (patients with recurrent ischemia, dynamic ECG changes, or hemodynamic instability). Abciximab, tirofiban, and eptifibatide appear to have equivalent efficacy, and the choice of drug should depend on other factors (e.g., cost, availability, familiarity). This agent is continued for 6 to 24 h.

Chest pain can be treated with nitroglycerin or sometimes morphine. Nitroglycerin is preferable to morphine, which should be used judiciously (e.g., if a patient has a contraindication to nitroglycerin or is in pain despite nitroglycerin therapy). Nitroglycerin is initially given sublingually, followed by continuous IV drip if needed. Morphine 2 to 4 mg IV, repeated q 15 min as needed, is highly effective but can depress respiration, can reduce myocardial contractility, and is a potent venous vasodilator. Evidence also suggests that morphine use interferes with some P2Y12 receptor inhibitors. A large retrospective trial showed that morphine may increase mortality in patients with acute myocardial infarction.

Hypotension and bradycardia secondary to morphine can usually be overcome by prompt elevation of the lower extremities.

Standard therapy for all patients with unstable angina includes beta-blockers, ACE inhibitors, and statins. Beta-blockers are recommended unless contraindicated (e.g. by bradycardia, heart block, hypotension, or asthma), especially for highrisk patients. Beta-blockers reduce heart rate, arterial pressure, and contractility, thereby reducing cardiac workload and oxygen demand. ACE inhibitors may provide long-term cardioprotection by improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not angioedema or renal dysfunction), an angiotensin II receptor blocker may be substituted. Statins are also standard therapy regardless of lipid levels and should be continued indefinitely.

Reperfusion therapy in acute myocardial infarction

For patients with STEMI: Immediate percutaneous coronary intervention or fibrinolytics. For patients with NSTEMI: Immediate percutaneous coronary intervention for unstable patients or within 24 to 48 h for stable patients. For STEMI patients, emergency PCI is the preferred treatment of ST-segment elevation myocardial infarction when available in a timely fashion (door to balloon-inflation time < 90 min) by an experienced operator. If there is likely to be a significant delay in availability of PCI, thrombolysis should be done for STEMI patients meeting criteria. Reperfusion using fibrinolytics is most effective if given in the first few minutes to hours after onset of myocardial infarction. The earlier a fibrinolytic is begun, the better. The goal is a door-toneedle time of 30 to 60 min. Greatest benefit occurs within 3 h, but the drugs may be effective up to 12 h. Characteristics and selection of fibrinolytic drugs are discussed elsewhere.

Unstable NSTEMI patients (i.e. those with ongoing symptoms, hypotension, or sustained arrhythmias) should proceed directly to the cardiac catheterization laboratory to identify coronary lesions requiring PCI or CABG.

For uncomplicated NSTEMI patients, immediate reperfusion is not as urgent because a completely occluded infarct-related artery at presentation is uncommon. Such patients typically undergo angiography within the first 24 to 48 h of hospitalization to identify coronary lesions requiring PCI or CABG. Fibrinolytics are not indicated for any NSTEMI patients. Risk outweighs potential benefit. Choice of reperfusion strategy is further discussed in Revascularization for Acute Coronary Syndromes.

Rehabilitation and post-discharge treatment

1-Functional evaluation.

2-Changes in lifestyle: Regular exercise, diet modification, weight loss, smoking cessation.

3-Drugs: Continuation of antiplatelet drugs, beta-blockers, ACE inhibitors, and statins.

Patients who did not have coronary angiography during admission, have no high-risk features (e.g., heart failure, recurrent angina, ventricular tachycardia or ventricular fibrillation after 24 h, mechanical complications such as new murmurs, shock), and have an ejection fraction > 40% whether or not they received fibrinolytics usually should have stress testing of some sort before or shortly after discharge.

The acute illness and treatment of myocardial infarction should be used to strongly motivate the patient to modify risk factors. Evaluating the patient’s physical and emotional status and discussing them with the patient, advising about lifestyle (e.g. smoking, diet, work and play habits, exercise), and aggressively managing risk factors may improve prognosis.

On discharge, all patients should be on appropriate anti-platelet drugs, statins, anti-anginals, and other drugs based on comorbidities [20] . Chewed aspirin [325 mg], and pain management with nitrates can reduce risk of mortality and complications. Early diagnostic data and response to treatment can help determine the need for and timing of revascularization.

Urgency for health care policy and research encompasses this contemporary concept:

1) Cardiac rehabilitation

2) Secondary prevention services are comprehensive, long term programs involving: medical evaluation, exercise, cardiac risk modification, education, counseling, this program are designed to limit:

1-The physiological and psychological effect of cardiac illness.

2-Reduce the risk factor for sudden death or re infraction.

3-Control cardiac symptoms.

4-stabilize or reverse the atherosclerotic process.

5-enhance the psych-social and vocational status of selected patient [15] . Although lack the power to change such as family history, sex, age, there are some key heart diseases prevention steps:

1-Smoking cessation significantly reduces the risk of dying from tobacco related disease (26) within 1 years coronary artery disease is cute in half [2] .

2-Exercises for about 30 minutes on most day of the week physical activity can reduce the risk of cardiovascular disease by control weight, reduces chances of developing other condition that put strain on the heart such as high BP, high cholesterol land diabetes [21] [22] .

3-Heart-healthy diet.

Two examples of heart healthy-food planes including:

1-dietary approaches to stop HTN (DASH) eating plane.

2-Mediterranean diet: diet rich in fruits, vegetables, whole grain, limited or avoid saturated fat and tans fat.

3-Manage of stress some people cope with stress in un healthy ways such as over eating, drinking or smoking so alternative ways to managed stress such as physical activity, relaxation, exercise [21] [22] .

Secondary prevention drug therapy:

1-aspirin and clopidogrel:

? For most low risk patients low to medium dose aspirin 75 - 325 mg.

? reduce risk of future infarction and other vascular events by approximately 25%. if patient are intolerant of long term aspirin clopidogrel is suitable alternative [2] [23] .

2-several trials have shown that long term treatment with ACEI can counteract:

3) Ventricular remodeling, reduce recurrent MI, Prevent the onset of heart failure, reduce re-hospitalization and improve survival so they should therefore be considered in all patients with ACS [2] .

3-lipid lowering drugs such as statin:

Lowering cholesterol in people of high risk of ischemic heart disease [23] .

4-coronary revascularization, for all patient at moderate or high risk.

It is associated & short & long term benefits including reduction in myocardial infarction &death.

5-implantable cardiac defibrillators: prevents sudden cardiac death in patients who have severe left ventricular impairment [2] .

Scanning patients of both gender who were diagnosed and treated as a case of myocardial infarction were incorporated into this study.

This study was conducted in Thamar governorate, Ma’bar City, Yemen, of AL-wahdah teaching hospital, Thamar University, Internal medicine Department.

This study was retrospective conducted from January 2018 to June 2021.

This study included 120 patients diagnosed as a case of MI and Subjected to treatment in AL-wahdah teaching hospital.

20 cases were excluded due to incomplete data or empty file.

Approval for this study was obtained from Thamar University Medical Ethics committee (TUMEC), in addition the approval was made by our supervisors.

This study was obtained from patients files who were diagnosed and treated as a cases of MI.

The related data was taken from each file and recorded in special Sheet designed for this purpose.

Data were entered and analyzed by using statistical package for social sciences (SPSS).

Acute MI above 40 years is becoming raising problem in Thamar city which is more common in men. The commonest risk factor of MI was Hypertension and the chest pain which is most common clinical presentations.

STEMI was the commonest type of MI in our study.

This study recommends that:

1) The Ministry of Health to perform many of its duties, carry out awareness campaigns to raise the level of the community culture about the tobacco related diseases and the necessity to smoking cessation.

2) Medical contributions from specialists in writing and circulating publications among members of the community about the importance of exercises and free fatty diet as a food rich in fibers on the health of the heart and body.

3) Routine screening which would help in preventing MI in risky patients.