Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack is the interruption of blood supply to part of the heart, causing some heart cells to die. This is most commonly due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia and oxygen shortage [1].

Acute myocardial infarction (AMI) is one of the most common human diseases and one of the leading causes of emergency department (ED) admission worldwide [2].

It is believed there is a diurnal variation in many systems in the body, including daily, monthly, and seasonal ones [3]. There are many studies describe the association between seasons and coronary artery disease as well as acute myocardial infarction [4].

The association between cardiovascular mortality and temperature is important, there are few studies have investigated the association between the incidence of cardiovascular disease (CVD) and temperature. Many of these studies that have examined the association between temperature and myocardial infarction (MI) have used mortality as an outcome rather than non-fatal events. Moreover, few of these studies have adjusted for potentially important confounders, such as (air pollution) [5]. Such variations can be of more significance when it comes to specific critical situations. For example, it has been found that the mortality rate in the wake of cardiopulmonary arrest is higher in winter than in summer [6].      Acute myocardial infarction has a seasonal variation, with higher frequency being reported in spring and winter. More recent studies confirmed these findings, observing that the frequency of AMI show a winter peak and summer [7].

Aims Of the Study

The aim of the study is to determine seasonal distribution and other epidemiological variables for patient with myocardial infarction admitted to coronary care unit in Baqubah teaching hospital in Diyala Province.

Literature Review

Historical Perspectives: After William Heberden’s classic description of angina pectoris in 1772, it took more than a century before pathologist Ludvig Hektoen in 1879 concluded that myocardial infarction is caused by coronary thrombosis secondary to sclerotic changes in the coronaries [9].

In 1910, the Russian clinicians Obrastzov and Straschesko published the first description of a nonfatal myocardial infarction. Two years later James B. Herrick published a paper, informing the American physicians about the symptoms of heart infarction based on the Russian paper, He further stimulated clinical use of the electrocardiogram as a diagnostic tool, and he emphasized “total bed rest” as the treatment for acute myocardial infarction (AMI). These approaches were standard care of patients with AMI until the beginning of the 1950s. Hospital mortality was high, more than 30%, and only morphine, and later diuretics and anticoagulants were used [9].

The first studies appeared in 1937 found an increase in mortality from acute myocardial infarction during the winter season; later studies carried out in North America, Asia, and Europe confirmed these finding [10].

In 1937 studies done, almost all continents have indicated that weather plays an important role in the onset of cardiovascular disease. The short-term effect on both cardiovascular morbidity and mortality has been evaluated through various reports [11].

Several researchers have focused their attention on acute myocardial infarction, which is a common CV disease that requires emergency medical treatment. In the past the effect of ambient temperature on AMI morbidity has received less attention [12].

Definition

The first WHO 1959 definition and other early definitions: The definition of acute myocardial infarction (AMI) was introduced by the World Health Organization (WHO) in 1959 with emphasis on chest pain and changes in successive ECGs [13].

It was followed by reports from American Heart Association (AHA) in 1964 and the WHO in 1971, and the Framingham study provided further specifications [14].

The diagnosis of AMI was based on the presence of at least two of three criteria: typical symptoms, typical ECG abnormalities and increase in enzymes indicating myocardial injury. WHO revised the diagnosis of ischemic heart disease in 1979 (WHO 1979 definition) with introduction of definite and possible AMI [13].

Factors Influencing the Seasonal Patterns of Cardiovascular Diseases

Temperature

Mechanisms that could explain the effect of temperature on cardiovascular diseases remain undetermined. In response to cold temperatures Activation of the sympathetic nervous system and secretion of catecholamine are increased. This could result in an increase in blood pressure through increased heart rate and peripheral vascular resistance [15].

Vitamin D

Significant seasonal vitamin D level variations were observed in several countries, which report a variation of values for 25-(OH) D, increased during summer and spring, while gradually decreasing in autumn and winter. Deficiency in Vitamin D level has been to be associated with CVD risk factors such as hypertension and diabetes mellitus, with markers of subclinical atherosclerosis such as intima-media thickness and coronary calcification as well as with cardiovascular events such as myocardial infarction, stroke and congestive heart failure [16].

Serum Cholesterol Level

Elevated level of Serum cholesterol has been shown to be associated with an increased risk for development of and death due to CVD. Serum cholesterol has strong relation with endothelial dysfunction and reduced nitric oxide bioavailability interestingly, a significant seasonal variation in plasma levels cholesterol has been reported in many studies, with maximum incidence in winter and minimum incidences in summer.

In Both Sexes

All levels of physical activity are significantly higher in summer than in winter, the positive effect of physical activity on CVDs remains unclear. One of these mechanisms through which physical activity is thought to affect CVDs is through improves endothelial function. The functions of endothelium are (maintain normal vasomotor tone, enhance the fluidity of blood and regulate vascular growth). Any Abnormalities in these functions cause many disease processes, including myocardial infarction, coronary vasospasm and hypertension. The other mechanism of exercise is increase in blood flow leading to increased shear stress, which is the force acting parallel to blood vessels. Enhanced shear stress results in endothelium-dependent, flow-mediated dilation of vessels. Chronic increases in shear stress have been found to improve endothelial function in animal studies as well as in some limited human studies [17].

Another mechanism proposed that the physical activity may also decrease the elevated sympathetic nerve activity that is common in essential hypertension [18].

Plasma Fibrinogen Levels

In the past decade many evidence has been accumulated which shows that the elevated plasma fibrinogen levels and factor VII clotting activity (FVIIc) had a strong and consistent association with cardiovascular disorders such as ischemic heart disease, stroke and peripheral vascular disease. Interestingly, seasonal variability with peak concentrations during winter months was shown for fibrinogen and FVIIc [19].

Seasonality of AMI

This was found in most age groups and both sex, men consistently exhibiting a stronger seasonality pattern, although the difference between both sex decreases with advancing age, cardiovascular deaths due to myocardial infarction account for the leading number of deaths among women as well as men, significant incidence relative ratios were found higher in males than female [20].

Dietary Intake

It is different in summer and winter as well as body mass index (BMI) and serum cholesterol, several epidemiological studies have demonstrated the relation between CVDs, overweight, high blood pressure and elevated serum total cholesterol. A significant and consistent relationship was shown between increase plasma total and LDL cholesterol and the incidence of CHD.

Myocardial Infarction

Signs and Symptoms: The onset of symptoms of myocardial infarction (MI) is usually gradual (over several minutes), and rarely suddenly (National Heart, Lung and Blood Institute. 2006). The most common symptom of acute myocardial infarction is chest pain and is often described as a sensation of tightness, pressure, or squeezing. Angina pectoris it defines as Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle. Pain radiates mostly to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastric area, where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their first over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value [21].

Dyspnea occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely due to a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities which result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and even sudden death (due to ventricular fibrillation) can occur in myocardial infarctions [22].

Women and old aged patients experience atypical symptoms more frequently than the male and young age counterparts; the women also have more symptoms compared to men (2.6 on average vs 1.8 symptoms in men) [23].

(Dyspnea, weakness, and fatigue) are the most common symptoms of MI in women. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event occurs. Chest pain may be less predictive of coronary ischemia in women than in men.

Approximately half of all MI patients have experienced warning symptoms like chest pain before the infarction occur and one fourth of all myocardial infarctions are silent, without chest pain or other symptoms [24]. These cases can be discovered later on using electrocardiograms, blood enzyme tests or at autopsy without a prior history of related complaints, A silent myocardial infarction is more common in the elderly, in patients with diabetes mellitus and after heart transplantation( probably because the donor heart is not connected to nerves of the recipient) [25].

In diabetic patients, differences in pain threshold, autonomic neuropathy, and psychological factors have been considered as possible explanations for the lack of symptoms (Davis, T. M. E. et al., 2004).

Risk factors of Myocardial Infarction

Many of the risk factors for myocardial infarction are modifiable and therefore many cases can be preventable.

Lifestyle

Smoking cause about 36% of coronary artery disease and obesity the cause of 20% of coronary artery disease, lack of exercise has been cause about 7 - 12% of cases; less common causes include stress-related causes such as job stress, which accounts for about 3% of cases and chronic high levels of stress [26].

Other life style risk factors include tobacco smoking (including secondhand smoke) and short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide, and sulfur dioxide (but not ozone) have been associated with MI [27].

There are other factors that increase the risk of MI and are cause worse outcomes after an MI include lack of physical activity and psychosocial factors including(low socioeconomic status, social isolation, and negative emotions, even shift work is also associated with a higher risk of MI), drinking high quantities of alcohol for acute and prolonged periods (3-4 or more) increase the risk of a heart attack [28].

The evidence for role of saturated fat is unclear. Some say there is benefit from reducing saturated fat in diet, and benefit from eating polyunsaturated fat instead of saturated fat, while others state there is little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake change heart attack risk [29].

Dietary cholesterol have a little effect on blood cholesterol and thus recommendations about its consumption may not be needed, while trans fats appear to increase risk of heart attack [29].

Disease

Diabetes mellitus (type 1 or 2), high blood pressure, dyslipidemia including high levels of blood cholesterol, abnormal levels of lipoproteins in the blood, particularly high (low-density lipoprotein), low (high-density lipoprotein) high triglycerides, in women under the age of 40 (endometriosis) and obesity (defined as body mass index of more than 30 kg/m²) have all been linked to MI [30].

There are a number of acute and chronic infections have been linked to atherosclerosis and myocardial infarction including Chlamydophila pneumoniae, influenza, Helicobacter pylori and Porphyromonas gingivalis, as of 2013, there is no evidence of benefit from antibiotics or vaccination, however, the association between heart disease and infections calling into question, myocardial infarction can also occur as a late consequence of Kawasaki disease [31]

Genetic

Genome-wide association studies have found 27 genetic variants that are associated with an increased risk of myocardial infarction, strongest association of MI has been found with the 9p21 genomic locus, which contains genes CDKN2A & 2B, although the single nucleotide polymorphisms that are implicated are within a non-coding region, the majority of these variants are in regions that have not been previously implicated in coronary artery disease ,the following genes have an associationwith MI: PCSK9, SORT1,MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1, CDKN2A, 2B, ABO, PDGF0, APOA5, MNF1AS M283, COL4A1, HHIPC1, SMAD3, ADAMTS7, RAS1, SMG6,SNF8, L DLR, SLC5A3, MRPS6, KCNE2 [32].

At any given age, men are more effected than women, particularly before menopause, but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women ,also family history of ischemic heart disease or MI increase risk of MI, especially if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women) [25].

Combined oral contraceptive pills have been found a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking, heart attacks appear to occur more commonly in the early morning hours, especially between 6AM and noon, there are evidence suggests that heart attacks are at least 3 times more likely to occur in the morning than in the late evening [34].

Pathophysiology of Myocardial Infarction

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated and ST-elevated MIs, which are most frequently (but not always) a manifestation of coronary artery disease [35].

The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery [36].

Atherosclerosis is defined as gradual buildup of cholesterol and fibrous tissue in plaques in the wall of coronary arteries [37].

Irregularities in blood vessels visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis [38].

Plaques can be unstable, rupture, and additionally promote the formation of blood clot that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary arteries, it will leads to MI (necrosis of downstream myocardium) [39]. It is estimated that one billion of cardiac cells are lost in a typical MI [40].

If blood flow to the heart impaired for long time, it triggers a process called the ischemic cascade; the heart cells in the region of the occluded coronary artery die(chiefly through necrosis) and do not grow back and collagen scar forms in their place. Recent studies found that there is another form of cell death (apoptosis), also plays a role in the process of tissue damage following an MI [41].

As a result of cell death, the heart muscle will be permanently damaged, this myocardial scarring also puts the person at risk for potentially life- threatening abnormal heart rhythms (arrhythmias), and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences [42].

The damaged heart tissue conducts electrical impulses more slowly than normal heart tissue, the difference in velocity of conduction between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious arrhythmia is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause sudden death also [43].

However, ventricular tachycardia can cause rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may decrease to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.

Pathological Types

There are two basic types of acute myocardial infarction which are:

Transmural

Transmural in which atherosclerosis involving major coronary artery. It can be classified into anterior, posterior and inferior. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the blood supply of this area [44].

Sub-Endocardial

Sub-endocardial in which infarction involves small area sub-endocardial wall of the left ventricle, ventricular septum, or papillary muscles. Sub-endocardial infarcts are thought to be result from locally decreased blood supply, possibly from a narrowing of the coronary arteries. Because of the sub-endocardial area is farthest from the heart's blood supply so it is more susceptible to this type of pathology. Clinically, myocardial infarction is further classified according to ECG changes into ST elevation MI and non-ST elevation MI [45].

Diagnosis of Myocardial Infarction

The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage [46]. A coronary angiogram can be used as diagnostic and therapeutic measures, its allow visualization of narrowing's or obstructions of the heart vessels, a chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department, Echo may be performed in equivocal cases by the cardiologist [31].

In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress [32].

Other diagnostic method, (Thallium) can be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of stasis or of being stunned [42].

The diagnostic criteria (WHO) criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two criteria (probable) or three criteria (definite) are present: Clinical history of ischemic type of chest pain lasting for more than 20 minutes; serial ECG Changes, increase serum cardiac biomarkers such as creatine kinase-MB fraction and troponin [47].

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers, according to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI [48].

Management of Myocardial Infarction

An MI requires immediate medical attention, treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is heart muscle".

Aspirin and nitroglycerin may be given to the patient. Nitroglycerin (administered either under the tongue or intravenously) to improve the blood supply to the heart [49].

In the past, high flow oxygen was used for everyone with possible myocardial infarction, recently routine use was found to lead to increased mortality and infarction size, therefore oxygen is now only used if oxygen levels are found to be low or the patient is in respiratory distress [49].

TEMI

The main treatments for ST elevation myocardial infarction (STEMI) are thrombolysis and percutaneous coronary intervention [50].

The treatment of choice for STEMI is Primary percutaneous coronary intervention (PCI) if it can be performed in a timely manner [51].

The second line of therapy if PCI cannot be performed within 90 to 120 minutes was thrombolysis, preferably given within 30 minutes of arrival to hospital, is recommended [52]. If the patient has had symptoms for 12 to 24 hours benefit of thrombolysis is less and if they have had symptoms for more than 24 hours it is not recommended [53].

NSTEMI

If there is no ST elevation, diagnosis of MI can confirmed by blood test for cardiac biomarkers (usually troponin). It can take 3–6 hours after the onset of symptoms to become positive, is referred to as "non-ST elevation acute coronary syndrome" (NSTEACS). In the meantime, the calculated risk of further cardiovascular events (e.g. using the GRACE score), the presence of other ECG changes and clinical features determines ongoing management [49].

Patient with an acute coronary syndrome with no ST elevation on ECG are treated with aspirin, Clopidogrel is added in many cases, especially if the risk of cardiovascular events is felt to be high and early PCI is being indicated.

Complications of Myocardial Infarction

Complications may be acute occur (immediately following the infarction), or may be chronic (need time to develop), after an infarction, one of important complication is a second infarction, which may occur in other atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Congestive heart failure following a myocardial infarction the function of the heart may be compromise as a pump for the circulation, this condition called heart failure. There are different types of heart failure; left and right-sided (or bilateral) heart failure may occur depending on the affected side of the heart, and it is a low-output type of failure, If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles, the incidence of heart failure is particularly high in diabetic patient and requires special management protocol [54].

Myocardial rupture is most commonly occur three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the area where early revascularization and intensive pharmacotherapy available as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs. The rupture may occur in the free walls of the ventricles, the septum between ventricles, the papillary muscles, or less commonly the atria. Rupture occurs due to increased pressure against the weakened walls of the heart chambers because of the heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm, a localized dilation or ballooning of the heart chamber [55].

Arrhythmia because of the electrical characteristics of the infarcted tissue change (describe in pathophysiology section), so arrhythmias are a frequent complication. The re-entry phenomenon may cause rapid heart rates (ventricular tachycardia and even ventricular fibrillation), and if the ischemia occur in the electrical conduction system of the heart it may cause a complete heart block (the impulse from the sinoatrial node which is the normal cardiac pacemaker not reach the heart chambers) [56].

Pericarditis as a result to the damage of the heart muscle, inflammatory cells are attracted and the inflammation may reach out and affect the heart pericardium. This is called pericarditis, in Dressler's syndrome, this occurs several weeks after myocardial infarction [57].

Cardiogenic shock this complication may occur either in acute setting soon after a myocardial infarction or in the weeks following it. Cardiogenic shock is a hemodynamic state in which the heart cannot pump enough cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body [58].

Patients and Methods

Patient Selection: This is a Retrospective study of (588) patients records with acute coronary syndrome admitted to the coronary care unit in Baqubah Teaching Hospital, for the period from 1^st January 2014 to 31^st December 2015, Baqubah Teaching Hospital located in Baqubah City center of Diyala, the bed capacity is (21) in the coronary care unit.

Data are collected from the case records according especial designed questionnaire form (Appendix), the data of patients are analyzed through gathering the data of climate temperature, resting electrocardiogram, biochemical markers, serum enzyme levels, serum lipid levels, and prior history of cardiac disease and coronary risk factors.

Weather

Mean monthly temperature data for the Baqubah Regional Office are obtained from the Bureau of Meteorology in the Iraqi Ministry of agriculture website, the mean monthly temperatures are derived from records for this site from (2014-2015).

Inclusion Criteria

The diagnostic criteria according to records a patient is diagnosed with myocardial infarction if two criteria (probable) or three criteria (definite) of the following are present: Clinical history of ischemic type chest pain lasting for more than 20 minutes; serial ECG Change ,increase serum cardiac biomarkers such as creatine kinase-MB fraction and Troponin.

Exclusion Criteria

Records of Patients with stable angina, valvular heart disease and old myocardial infarction are excluded from the study.

Statistical Analysis

Analysis of collected information is done by computer software and the results of this descriptive study presented by numbers and percentages.

Seasonal Distribution

Total No. of cases are (588) case of myocardial infarction, most admission occur during winter, (202 case 34.3%), and spring (155 case 26.3 %) as shown in Table 1.

Table 1: Distribution of the Patients with Myocardial Infarction According to the Seasons of the Year and It Temperature (Max-Min)

Gender Distribution

Most common effected gender is male (434 cases 73.80%) and most admission occur in winter (151 cases 25.6%) while female (154 cases 26.20%) and most admission occur in winter (51 cases 8.6%) as shown in Table 2.

Table 2: Seasonal Distribution of Admitted Patients According to Gender

Age Distribution

Patients age ranged between (21 - 90) years, the most commonly age group involved were between (51 - 60) 187 case (31.8%) as shown in Table 3.

Table 3: Distribution of Myocardial Infarction According to the Age

Occupation of Patients

Retired are most frequent occupations among the patients with AMI 183 cases (31.12%) as shown in Table 4.

Table 4: Distribution of Myocardial Infarction According to the Occupation of The Patients

Risk Factors

Smoking is the most affected risk factor in myocardial infarction 272 cases (46.25%), then diabetes (249 cases 42.34%) and hypertension (242 cases 41.15%) as shown in Table 5.

Table 5: Distribution of Patients According to Risk Factors

Mortality

Total No. of death was (121 dead 20.5%), mortality rate more in male than female and most of death occur in Spring (40 dead 33.05%) and Winter (36 dead 29.7%) as shown in Table 6.

Table 6: Mortality of Patients According to the Months of The Year

Seasonal Distribution

Total numbers of records are (588) of myocardial infarction, most admission occurs during winter 202 (34.3%) and Spring 155 (26.3 %).

This result agrees with the study of how revealed the highest incidence of AMI to be in January and lowest in august.

Using data from a Korean AMI registry, the monthly prevalence was found to be highest in January and lowest in October [59].

Coronary events are more obvious in winter because of possible changes in the blood pressure caused by decrease temperature or in consequence of changes in the levels of fibrinogen, which may be induced by winter respiratory infections that can activate the acute phase reactants, Life style risk factors are likely to have a role as well [19].

There are Another potentially important risk factors such as seasonal variation in the plasma level of fibrinogen, cholesterol, Hormones and vasoactive substance including vasopressin (AVP), nor epinephrine (NE), epinephrine (E) and angiotensin II, aldosterone and catecholamine which tends to increase in the winter is suggested to play an important role in the seasonal change of coronary diseases [60].

Gender

Most of the sample in my study was males; they represent about (73.8%) of our study, while females were (26.2%).

This result agree with study in Nablus was done by [61] who found the most affected gender is male. Men have a greater risk of coronary disease than women at all ages, and they have attacks earlier in life. Even after menopause, when women's death rate from heart disease increases, it's not as great as men's.

Age

Most of the sample in the study was at fifth decade (31.8%); followed by sixth decade (23.8%).

The result of this study agrees with the result of [62] who found that the average age of onset of MI was (59.18 + 10.8) years.

These results were expected because age is considered as one of the major risk factors of myocardial infarction, over 83% of people who die of coronary heart disease are 65 or older.

Occupation

In this study retired patients are most affected group among the patients with AMI 183 (31.12%) which is mean most probably that the person with low physical activity is more susceptible to AMI. This result agrees with Noda, H. et al. [63] and the study of [64].

Risk Factors

In this study smoking is the most effected risk factor in myocardial infarction 272 (46.25%), then diabetes 249 (42.34%) and hypertension 242 (41.15%). This result agrees with [64]. Cigarette smoking increases the risk of coronary heart disease. And when there are other factors associated with it, the risk will greatly increase. Smoking increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot.

1. Kosuge, M. et al. "Differences between men and women in terms of clinical features of st-segment elevation acute myocardial infarction." Circulation Journal, vol. 70, no. 3, 2006, pp. 222–26.

2. Boyle, A. et al. "Emergency department crowding: Time for interventions and policy evaluations." Emergency Medicine International, 2012.

3. Konuralp, C. et al. "Effects of seasonal variations on coronary artery surgery." The Heart Surgery Forum, vol. 5, no. 4, 2002, pp. 388–92.

4. Spencer, F.A. et al. "Seasonal distribution of acute myocardial infarction in the second national registry of myocardial infarction." Journal of the American College of Cardiology, vol. 31, no. 6, 1998, pp. 1226–33.

5. Bhaskaran, K. et al. "Effects of ambient temperature on the incidence of myocardial infarction." Heart, vol. 95, no. 21, 2009, pp. 1760–69.

6. Pell, J.P. and S.M. Cobbe. "Seasonal variations in coronary heart disease." QJM, vol. 92, no. 12, 1999, pp. 689–96.

7. Lee, J.H. et al. "Influence of weather on daily hospital admissions for acute myocardial infarction." International Journal of Cardiology, vol. 144, no. 1, 2010, pp. 16–21.

8. Nabel, E.G. and E. Braunwald. "A tale of coronary artery disease and myocardial infarction." New England Journal of Medicine, vol. 366, no. 1, 2012, pp. 54–63.

9. de Vreede, J.J. et al. "Did prognosis after acute myocardial infarction change during the past 30 years? a meta-analysis." Journal of the American College of Cardiology, vol. 18, no. 3, 1991, pp. 698–706.

10. Douglas, A.S. et al. "seasonal variation in coronary heart disease in scotland." Journal of Epidemiology and Community Health, vol. 49, no. 6, 1995, pp. 575–82.

11. Braga, A.L. et al. "The effect of weather on respiratory and cardiovascular deaths in 12 us cities." Environmental Health Perspectives, vol. 110, no. 9, 2002, pp. 859–63.

12. Wichmann, J. et al. "Apparent temperature and acute myocardial infarction hospital admissions in copenhagen, denmark." Environmental Health, vol. 11, no. 1, 2012, pp. 1–12.

13. World Health Organization. Hypertension and Coronary Heart Disease: Classification and Criteria for Epidemiological Studies. WHO, 1959.

14. Weinstein, B.J. et al. "Comparability of criteria and methods in the epidemiology of cardiovascular disease." Circulation, vol. 30, no. 5, 1964, pp. 643–53.

15. Hanna, J.M. "Climate, altitude, and blood pressure." Human Biology, 1999, pp. 553–82.

16. Gouni-Berthold, I. et al. "Vitamin D and Cardiovascular Disease." Current Vascular Pharmacology, vol. 7, no. 3, 2009, pp. 414–22.

17. Sherman, D.L. "Exercise and endothelial function." Coronary Artery Disease, vol. 11, no. 2, 2000, pp. 117–22.

18. Pescatello, L.S. et al. "Exercise and hypertension." Medicine & Science in Sports & Exercise, vol. 36, no. 3, 2004, pp. 533–53.

19. Woodhouse, P.R. et al. "Seasonal variations of plasma fibrinogen and factor vii activity in the elderly." The Lancet, vol. 343, no. 8895, 1994, pp. 435–39.

20. Takigawa, M. et al. "Seasonal and circadian distributions of ventricular fibrillation in patients with brugada syndrome." Heart Rhythm, vol. 5, no. 11, 2008, pp. 1523–27.

21. Marcus, G M. et al. "The utility of gestures in patients with chest discomfort." The American Journal of Medicine, vol. 120, no. 1, 2007, pp. 83–89.

22. Little, R.A. et al. "Plasma catecholamines in the acute phase of the response to myocardial infarction." Emergency Medicine Journal, vol. 3, no. 1, 1986, pp. 20–27.

23. Canto, J.G. et al. "Symptom presentation of women with acute coronary syndromes." Archives of Internal Medicine, vol. 167, no. 22, 2007, pp. 2405–13.

24. Lee, D. et al. "Heart attack (Myocardial Infarction)." MedicineNet, 2006.

25. Wilson, P.W. et al. "Prediction of coronary heart disease using risk factor categories." Circulation, vol. 97, no. 18, 1998, pp. 1837–47.

26. Kivimäki, M. et al. "Job strain as a risk factor for coronary heart disease." The Lancet, vol. 380, no. 9852, 2012, pp. 1491–97.

27. Mustafić, H. et al. "Main air pollutants and myocardial infarction." JAMA, vol. 307, no. 7, 2012, pp. 713–21.

28. Krenz, M. and R. J. Korthuis. "Moderate ethanol ingestion and cardiovascular protection." Journal of Molecular and Cellular Cardiology, vol. 52, no. 1, 2012, pp. 93–104.

29. De Souza, R.J. et al. "Intake of saturated and trans fatty acids and risk of cardiometabolic disease." BMJ, 2015.

30. Yusuf, S. et al. "Obesity and the risk of myocardial infarction in 27,000 participants." The Lancet, vol. 364, no. 9438, 2005, pp. 937–52.

31. Sánchez-Manubens, J. et al. "Diagnosis and classification of kawasaki disease." Journal of Autoimmunity, vol. 48, 2014, pp. 113–17.

32. O'Donnell, C.J. and E.G. Nabel. "Genomics of cardiovascular disease." New England Journal of Medicine, vol. 365, no. 22, 2011, pp. 2098–108.

33. Shaw, E. and G.H. Tofler. "Circadian rhythm and cardiovascular disease." Current Atherosclerosis Reports, vol. 11, no. 4, 2009, pp. 289–95.

34. —. "Circadian Rhythm and Cardiovascular Disease." Current Atherosclerosis Reports, vol. 11, no. 4, 2009, pp. 289–95.

35. Moe, K.T. and P. Wong. "Current trends in diagnostic biomarkers of acute coronary syndrome." Annals of the Academy of Medicine, Singapore, vol. 39, no. 3, 2010, pp. 210–15.

36. Tsujita, K. et al. "Acute coronary syndrome–initiating factors." Nihon Rinsho, vol. 68, no. 4, 2010, pp. 607–14.

37. Woollard, K. J., and F. Geissmann. "Monocytes in Atherosclerosis." Nature Reviews Cardiology, vol. 7, no. 2, 2010, pp. 77–86.

38. Spaan, J. et al. "Coronary structure and perfusion in health and disease." Philosophical Transactions of the Royal Society A, vol. 366, no. 1878, 2008, pp. 3137–53.

39. Dohi, T. and H. Daida. "Change of concept and pathophysiology in acute coronary syndrome." Nihon Rinsho, vol. 68, no. 4, 2010, pp. 592–96.

40. Laflamme, M.A. and C.E. Murry. "Regenerating the heart." Nature Biotechnology, vol. 23, no. 7, 2005, pp. 845–56.

41. Krijnen, P. A. J., et al. "Apoptosis in Myocardial Ischaemia and Infarction." Journal of Clinical Pathology, vol. 55, no. 11, 2002, pp. 801–11.

42. Wilson, A.M. et al. "The novel role of c-reactive protein in cardiovascular disease." International Journal of Cardiology, vol. 106, no. 3, 2006, pp. 291–97.

43. Pearson, T.A. et al. "Markers of inflammation and cardiovascular disease." Circulation, vol. 107, no. 3, 2003, pp. 499–511.

44. Reznik, A.G. "Morphology of acute myocardial infarction at prenecrotic stage." Kardiologiia, vol. 50, no. 1, 2010, pp. 4–8.

45. Antman, E. et al. "Myocardial infarction redefined." Journal of the American College of Cardiology, vol. 36, no. 3, 2000, pp. 959–69.

46. Charakida, M. and D. Tousoulis. "Infections and atheromatous plaque." Current Pharmaceutical Design, vol. 19, no. 9, 2013, pp. 1638–50.

47. Khader, Y.S. et al. "Oral contraceptives use and the risk of myocardial infarction." Contraception, vol. 68, no. 1, 2003, pp. 11–17.

48. Čulić, V. "Acute risk factors for myocardial infarction." International Journal of Cardiology, vol. 117, no. 2, 2007, pp. 260–69.

49. Amsterdam, E.A. et al. "2014 AHA/ACC Guideline for the management of patients with non–st-elevation acute coronary syndromes." Journal of the American College of Cardiology, vol. 64, no. 24, 2014, pp. e139–e228.

50. Bates, E.R. and D.S. Menees. "Acute st-elevation myocardial infarction." Current Opinion in Critical Care, vol. 18, no. 5, 2012, pp. 417–23.

51. Bagai, A. et al. "Reperfusion strategies in acute coronary syndromes." Circulation Research, vol. 114, no. 12, 2014, pp. 1918–28.

52. Lassen, J.F. et al. "Timely and optimal treatment of patients with STEMI." Nature Reviews Cardiology, vol. 10, no. 1, 2013, pp. 41–48.

53. Neumar, R. W., et al. "2015 AHA Guidelines Update for CPR and ECC." Circulation, vol. 132, no. 18, 2015, pp. S315–S67.

54. Canto, J.G. et al. "Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain." JAMA, vol. 283, no. 24, 2000, pp. 3223–29.

55. Shin, P. et al. "Postinfarction cardiac rupture: A pathogenetic consideration." Pathology International, vol. 33, no. 5, 1983, pp. 881–93.

56. Sung, R.J. and M.R. Lauer. Fundamental Approaches to the Management of Cardiac Arrhythmias. Springer, 2000.

57. Josephson, M.E. Clinical Cardiac Electrophysiology. Lippincott Williams & Wilkins, 2008.

58. Hochman, J.S. et al. "Early revascularization in acute myocardial infarction complicated by cardiogenic shock." New England Journal of Medicine, vol. 341, no. 9, 1999, pp. 625–34.

59. Lee, I.M. et al. "Effect of physical inactivity on major noncommunicable diseases worldwide." The Lancet, vol. 380, no. 9838, 2012, pp. 219–29.

60. Peters, A. et al. "Increased particulate air pollution and the triggering of myocardial infarction." Circulation, vol. 103, no. 23, 2001, pp. 2810–15.

61. Aubeidia, M.A.R.T. Assessment of Myocardial Infarction Risk Among Patients in Nablus District. Doctoral dissertation, 2006.

62. Saidi, S.J. and M. M. Kalantar. "Myocardial infarction: Factors influencing age of onset." 2005.

63. Noda, H. et al. "Walking and sports participation and mortality from coronary heart disease and stroke." Journal of the American College of Cardiology, vol. 46, no. 9, 2005, pp. 1761–67.

64. Breckenkamp, J. et al. "Questionnaire study of stroke, myocardial infarct and arterial occlusive disease." MMW Fortschritte der Medizin, vol. 145, no. 37, 2003, pp. 43–44.