Heart attack vs. stroke: What’s the difference?

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Two and a half weeks ago, AD experienced a stressful situation that caused him to lose sleep for two consecutive nights. Following this, he developed muscle weakness in his shoulder, which extended down to his left forearm. I advised him to consult his cardiologist, but unfortunately, he did not follow through. Instead, he took a pain reliever to ease the soreness in his left arm. This initially brought some relief, but after several days, the muscle weakness, fatigue, soreness, and achiness in his left arm returned.

At that time, he did not report any chest pain, chest heaviness, shortness of breath, lightheadedness, or nausea. However, about a week later, while at the mall, he experienced sudden paleness of his lips, chest heaviness, and shortness of breath. This time, the pain radiated from his jaw to his shoulder and extended down to his left forearm. Believing the pain might be due to a dental issue, he contacted his dentist, who prescribed another pain reliever. When that brought no relief, I strongly advised him to see his cardiologist Dr. James Ho and his nephrologist Dr. Agnes Mejia as soon as possible

He was eventually taken to the ER by his househelp, where several laboratory tests were conducted. Doctors determined that he needed to be admitted for close observation and further testing, as he was experiencing a myocardial infarction (heart attack).

It’s important to note that a myocardial infarction and a stroke, while both serious cardiovascular events, are not the same. A heart attack involves a blockage of blood flow to the heart muscle, whereas a stroke results from a blockage of blood flow to the brain. However, both conditions require immediate medical attention.

Myocardial infarction (MI) is sudden ischemia of the heart muscle tissue due to lack of or obstruction of coronary blood flow, which leads to its damage. Myocardial infarction (MI) results from a severe and prolonged imbalance between the myocardial O2 supply and its requirements. In most cases, this occurs as a result of occlusive coronary atherosclerosis (thickening or hardening of the arteries secondary to a buildup of plaque). Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin sometimes concomitant with bloot clot. Atherosclerosis is a dynamic, progressive process. Its effects are attributed to a combination of inflammation and endothelial dysfunction (damage of the inner lining of the artery). In about 10 percent of cases, myocardial infarction may occur without detection of coronary artery obstruction but may be due to: coronary artery spasm, plaque disruption, spontaneous coronary artery dissection, in-situ thrombosis and microvascular dysfunction. In these cases, it is important to rule out other causes of elevated troponin (a protein found in heart and skeletal muscle cells) such as myocarditis, Takotsubo cardiomyopathy and pulmonary embolism.

The central mechanism of the pathophysiology is the same regardless of the etiological factors that may only modify the outcome.

In 2001, there were about 7.3 million deaths from coronary heart disease (CHD). About three-quarters are encountered in low- and middle-income countries. It was noted that the mortality rate among males is higher than among females at young ages. However, it often converges with age.

Since the damage from myocardial infarction is irreversible, it is essential to properly diagnose and resuscitate the heart as soon as possible. The sooner treatment takes place less than six hours after symptoms appear, the better the prognosis. Knowledge of myocardial infarction risk causes, clinical manifestations, diagnosis and treatment is important in the accurate and rapid management of myocardial infarction.

Risk factors

Identification of RFs is important for approaches to preventing most premature MI. The RFs include smoking five or more cigarettes per day, diabetes with a blood glucose level of ≥126 mg/dL, hypertension, central obesity (big abdomen), and low-density lipoprotein cholesterol (bad cholesterol) from 100 to 120 mg/dL. However, there are other factors called non-modifiable RFs including age above 45 years for males and above 55 years for females, African-Americans race and previous family history of early CAD.

Smoking. Smoking is responsible for about 10 percent of deaths which is expected to increase to about 17 percent by 2030. Tobacco smoking increases blood pressure and heart rate, resulting in an increase in metabolic oxygen demand by the heart muscle. At the same time, it leads to narrowing of blood vessels, leading to a reduction in the size of the coronary arteries, decreasing blood flow to the heart muscle. These adverse effects can be exacerbated by concomitant use of cocaine.

Hypertension. Hypertension is an important risk factor for CAD and AMI. There is a direct association between high blood pressure values and morbidity and mortality of CAD.. With high blood pressure, the risk of developing AMI has been found to increase to more than twofold.

Diabetes mellitus. Diabetes mellitus (DM) is a well-documented risk factor for CAD and AMI. Myocardial infarction (MI) is more common in diabetic patients than in non-diabetics. Insulin resistance, hyperglycemia and excess fatty acids lead to increased systemic oxidative stress and inflammation as well as production of advanced glycation product. All of these factors contribute to the emergence and development of coronary atherosclerosis and microvascular impairment.

Anthropometric measures. Although body weight appears to predict obesity, its values do not differentiate between body fat and muscle mass. Moreover, central fat (fat in the abdominal area) has more to do with the development of atherosclerosis than peripheral obesity. Central obesity is a greater indicator in CAD risk than generalized obesity even in people of normal weight.

Blood lipids. The low-density lipoprotein (LDL)-cholesterol is associated with development of atherosclerosis, endothelial dysfunction and arterial plaques that represent the potential cause of CAD and stroke.

Inflammation. There are accumulating data that inflammation is considered a major risk factor for atherosclerosis development. Increased levels of highly sensitive C-reactive protein (CRP) could be an indicator of CHD risk in healthy individuals more than elevation of LDL values.

Alcohol intake. The effect of excessive drinking doubles the risk of developing AMI compared to not drinking alcohol. Such a benefit is thought to be achieved by increasing HDL (good cholesterol), rather than affecting platelets and fibrinolysis.

Socio-economic status. Socio-economic status is associated with CAD and AMI risks. Individuals with elementary school education are most affected, regardless of social class. Moreover, individuals with low incomes and material deprivation are exposed to excessive psychosocial stress that is detrimental to overall health including the cardiovascular system.

Family history. Family history, especially for first-degree relatives, is considered to be an independent risk factor for AMI. It has been claimed that about 40 to 60 percent of coronary heart disease is inherited. Therefore, taking a detailed family history may be necessary, especially in patients between 35 and 55 years of age, for appropriate assessment of AMI risk.

It has been found that moderate muscle exercise, regular consumption of fresh vegetables and fruits, avoidance of smoking and stress, and low consumption of fat are associated with a reduced risk of coronary heart disease in populations of all age groups worldwide.

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