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Table of Contents
REVIEW ARTICLE
Year : 2019  |  Volume : 4  |  Issue : 3  |  Page : 71-80

A scientific update on myocardial infarction: A life-threatening issue


Department of Pharmacology, School of Pharmacy, Babu Banarasi Das University, Lucknow, Uttar Pradesh, India

Date of Submission11-May-2019
Date of Acceptance18-Jun-2019
Date of Web Publication30-Sep-2019

Correspondence Address:
Mayank Kulshreshtha
Department of Pharmacology, School of Pharmacy, Babu Banarasi Das University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cp.cp_13_19

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  Abstract 


Cardiovascular diseases (CVDs) are the principal cause of mortality in India, 52% of population suffer CVDs before 70 years of age. Myocardial infarction (MI) makes up the largest proportion of CVDs. Coronary heart disease, namely stable angina pectoris, unstable angina pectoris, heart failure, and sudden death, is the main results of MI. The aim of this review is to summarize and present the scientific data regarding the physiology of the cardiac system, herbal research, risk factors, precautions, and pharmacological/nonpharmacological treatment of MI. Data were collected with the help of PubMed, Google Scholar, Medknow, and other online resources. The published scientific data revealed that MI is the result of obesity, smoking, family history, age, male gender, etc., and that the herbal resources are better than the synthetic or chemical treatment of MI. Because the synthetic molecules were not found to be safe, they can generate other health issues. Given problems with the pharmacological treatment of MI, precaution, and a good lifestyle is the better solution.

Keywords: Herbal therapy, lifestyle, myocardial infarction


How to cite this article:
Bhushan A, Kulshreshtha M. A scientific update on myocardial infarction: A life-threatening issue. Cardiol Plus 2019;4:71-80

How to cite this URL:
Bhushan A, Kulshreshtha M. A scientific update on myocardial infarction: A life-threatening issue. Cardiol Plus [serial online] 2019 [cited 2019 Dec 10];4:71-80. Available from: http://www.cardiologyplus.org/text.asp?2019/4/3/71/268291




  Introduction Top


There are variations in cardiac functioning from patient to patient according to bodily make-up or disease, and minor changes occur with respiration. In very rare circumstances, the entire bodily structure can be a mirror image in the setting of normality, or when there is an associated congenital cardiac malformation. In other circumstances, more common than the mirror-imaged situation, but still relatively rare, the structures of the body that usually demonstrate lateralization are arranged in isomeric fashion.[1] The human heart is a vital organ that continuously circulates blood throughout the body in cycles. The heart rests on the diaphragm, which is near the thoracic cavity. It lies in the mediastinum which is an anatomical region that exit from the sternum to the vertebral column (rib to the diaphragm and between the lungs). Heart always lies to the left of the body's midline about two-thirds. Pericardium surrounds and protects the heart. It helps in confining the heart to its position in the mediastinum, as well as allows sufficient freedom of movement for vigorous and rapid contraction. Three layers of the wall of the heart are the epicardium (external layer), the myocardium (middle layer), and the endocardium (inner layer). The heart has the two superior receiving chambers (known as atria) and the two inferior pumping chambers (known as ventricles).[2]


  Physiology of Cardiac Function Top


The heart chambers normally contract with properly coordinated manner means they pumping blood efficiently by a route determined by the valves. Coordination of contraction is called a specialized conducting system which is define impulses arising in the sinoatrial (SA) node and conducted in sequence through the atria, the atrioventricular (AV) node, bundle of His then Purkinje fibers and ventricles.[3] Heart cells owe their electrical excitability to voltage-sensitive plasma membrane channels selective for various ions, including Na +, K +, and Ca +. Electrophysiological features of cardiac muscle that distinguish it from other excitable tissues include pacemaker activity, absence of fast Na + current in SA and AV nodes, where slow inward Ca 2+ current initiates action potentials, long action potential (“plateau”) and refractory period, influx of Ca 2+ during the plateau. Different phases of the action potential are shown in [Table 1].[4]
Table 1: Different phases of the cardiac cycle

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  Myocardial Oxygen Consumption and Coronary Blood Flow Top


Relative to its large metabolic needs, the heart is one of the most poorly perfused tissues in the body. Coronary flow is, under normal circumstances, closely related to myocardial oxygen consumption, and both change over a nearly 10-fold range between conditions of rest and maximal exercise.

The main physiological factors that regulate coronary flow are as follows:

  • Physical factors
  • Vascular control by metabolites
  • Neural and humoral control.[5]


Physical factors

During systole, the pressure exerted by the myocardium on vessels that pass through it equals or exceeds the perfusion pressure, so coronary flow occurs only during diastole. Diastole is shortened more than systole during tachycardia, reducing the period available for myocardial perfusion. During diastole, the effective perfusion pressure is equal to the difference between the aortic and ventricular pressures. If diastolic aortic pressure falls or diastolic ventricular pressure increases, perfusion pressure falls, and so (unless other control mechanisms can compensate) does coronary blood flow. Stenosis of the aortic valve reduces aortic pressure, but increases left ventricular (LV) pressure upstream of the narrowed valve, and often cause ischemic chest pain (angina) even in the absence of coronary artery disease.[6]

Metabolic vasomotion

Metabolic vasomotion is the response of the coronary vasculature to changes in myocardial metabolism, which in turn are almost entirely a consequence of changes in myocardial performance. The mechanism(s) and signal mediators of metabolic coronary vasomotion have been a matter of debate over decades and are still not clearly understood.[7] Adenosine has attracted a lot of interest and is a mediator that intuitively has a logical charm, because the formation of adenosine in cardiomyocytes is stoichiometrically coupled to ATP breakdown, and its release and vasodilator action on coronary vascular smooth muscle cells can increase coronary blood flow and the delivery of oxygen and substrates and thus restore the myocardial energetic state.[8],[9] Likewise, the activation of ATP-dependent potassium channels on the surface membranes of coronary vascular smooth muscle cells would imply a certain coupling to the energetic state of smooth muscle cells rather than cardiomyocytes.[10],[11]

Neural and humoral control

Neurohumoral regulation of blood flow occurs in large coronary arteries and in the microcirculatin. However, neurohumoral factors can affect the endothelial, metabolic, and myogenic regulation of coronary blood flow. The large epicardial and intramyocardial coronary arteries are densely innervated by postganglionic sympathetic and parasympathetic nerve fibers. Therefore, norepinephrine and acetylcholine released from these fibers interact with coronary adrenergic and muscarinic receptors to control coronary vascular resistance.[12],[13],[14]


  Myocardial Infraction Top


Cardiovascular diseases (CVDs) are the main causes of human disability and mortality worldwide.[15] Myocardial infarction (MI) is commonly known as ischemic heart disease or heart attack; it is an irreversible necrosis of tissue of a region of the myocardium caused by ischemia.[16] Studies show that the pathophysiology mechanisms behind myocardial I/R injury are related to many factors, such as massive-free radical production, changes in hemorheology, intracellular calcium overload, increased inflammation, myocardial necrosis, and apoptosis.[17] Therefore, in the clinical setting, myocardial I/R injury is considered a major factor that affects patient outcome.

The evidence of MI can be identified by elevations of different proteins released into the blood by the damaged myocytes. These biomarkers include cardiac troponin T (cTnT) and cardiac troponin I (cTnI), creatine kinase MB isoenzyme (CK-MB), lactate dehydrogenase (LDH), and many others. The determination of cTnT or cTnI is a highly sensitive and specific analytical method for cardiac injury as these contractile proteins are released from myocardium during the myocardium tissue injury and disruption of myocyte membranes.[18] Main risk factors for the MI is the atherosclerosis of coronary artery,[19] calcium reduction, generation of free radicals, oxidative metabolism of catecholamines, these oxidative products impact on the cardiac myocyte membrane and also depress the cardiac contractile function, prior to which damage in the mitochondria, sarcotubular system, and contractile functions.[20]

Epidemiology

CVD remains the principal cause of death in developed and developing countries, claiming 17.1 million lives a year. According to the WHO, it is predicted that CVD will be the most important cause of mortality in India by 2020.[21] Among several CVDs particularly MI has become a worldwide health problem affecting all economic groups of the society and it continues to be a major public health problem, not only in western and industrialized countries but also increasingly in developing countries, such as India and makes a significant contribution to the mortality statistics. It is the leading cause of mortality for both men and women in developed and developing countries. In developed countries, MI accounts for 10%–25% of all deaths.[22]

Types

MIs are usually classified by size: microscopic (focal necrosis), small (<10% of the 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 the clinical history.

MIs can be classified temporally from clinical and other features, as well as according to the pathological appearance, as evolving (<6 h), acute (6 h–7 days), healing (7–28 days), and healed (29 days and beyond). Clinical classification of different types of MI include:[23]

Type 1

Spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection.

Type 2

MI secondary to ischemia due to either increased oxygen demand or decreased supply, for example, coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension.

Type 3

Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new LBBB (left bundle branch block), or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.

Type 4A

MI associated with percutaneous coronary interventions (PCIs).

Type 4B

MI associated with stent thrombosis as documented by angiography or at autopsy.

Type 5

MI associated with coronary artery bypass grafting.

Prevalence and risk factors

A heart attack happens if the flow of oxygen-rich blood to a section of heart muscle suddenly becomes blocked and the heart cannot get oxygen. Most heart attacks occur as a result of coronary heart disease; it is a condition in which a waxy substance called plaque builds up inside of the coronary arteries. These arteries supply oxygen-rich blood to your heart. When plaque builds up in the arteries, the condition is called atherosclerosis. The buildup of plaque occurs over many years. Eventually, an area of plaque can rupture (break open) inside of an artery. This causes a blood clot to form on the plaque's surface. If the clot becomes large enough, it can mostly or completely block blood flow through a coronary artery. If the blockage is not treated quickly, the portion of heart muscle fed by the artery begins to die. Healthy heart tissue is replaced with scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems. A less common cause of heart attack is a severe spasm (tightening) of a coronary artery. The spasm cuts off blood flow through the artery. Spasms can occur in coronary arteries that are not affected by atherosclerosis.[24]

Several factors may lead to a blockage in the coronary arteries:


  Hyperlipidemia Top


Elevated levels of total cholesterol, LDL, or triglycerides are associated with an increased risk of coronary atherosclerosis and MI. Levels of HDL <40 mg/dl also portend an increased risk.

Hypertension

High blood pressure (BP) has consistently been associated with an increased risk of MI. This risk is associated with systolic and diastolic hypertension. The control of hypertension with appropriate medication has been shown to reduce the risk of MI significantly.

Diabetes and high blood sugar levels

Patients with diabetes have a substantially greater risk of atherosclerotic vascular disease in the heart as well as in other vascular beds. Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects the lipid profile. This accelerated form of atherosclerosis occurs regardless of whether a patient has insulin-dependent or noninsulin-dependent diabetes.

Obesity

Chances of having a heart attack are higher in case of overweight. Obesity is associated with various conditions that increase the risk of heart attack.

Smoking

Smoking tobacco products increases the risk of heart attack. Certain components of tobacco and tobacco combustion gases are known to damage blood vessel walls. The body's response to this type of injury elicits the formation of atherosclerosis and its progression, thereby increasing the risk of MI.

Age

The risk of having a heart attack increases with age. Men are at a higher risk of a heart attack after the age of 45 years, and women are at a higher risk of a heart attack after the age of 55 years.

Family history

A family history of the premature coronary disease increases an individual's risk of atherosclerosis and MI. The cause of familial coronary events is multifactorial and includes other elements, such as genetic components and acquired general health practices (e.g., smoking and high-fat diet).

Male gender

The incidence of atherosclerotic vascular disease and MI is higher in men than women in all age groups. This gender difference in MI, however, narrows with increasing age.[24]

Symptoms

Acute MI can have unique manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. 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 chest pain described as a pressure sensation, fullness, or squeezing in the mid portion of the thorax.[25]

  • Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back
  • Associated dyspnea or shortness of breath
  • Associated epigastric discomfort with or without nausea and vomiting
  • Associated diaphoresis or sweating
  • Syncope or near syncope without other cause
  • Impairment of cognitive function without other cause
  • Anxiety
  • Cough
  • Dizziness
  • A fast heart rate.



  Pathophysiology Top


MI is defined by pathology as myocardial cell death due to prolonged ischemia. Cell death is categorized pathologically as coagulation and/or contraction band necrosis, which usually evolves through oncosis, but can result to a lesser degree from apoptosis.

Atherosclerotic plaques form gradually over the years. They begin with the accumulation of LDL cholesterol and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the adhesion of leukocytes to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to this point is referred to as a fatty streak and may be reversible to a certain extent.[3] Subsequent evolution involves the migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibers. Some of the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification as they evolve. The plaque initially evolves with the artery remodeling outwards, followed by encroachment on the arterial lumen. Eventually, the stenosis can limit flow under conditions of increased demand, causing angina. MI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results in exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial cell necrosis follows.[26]

On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the noninfarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank–Starling mechanism. As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction, leading to infarction expansion.[27] If a sufficient quantity of myocardium undergoes ischemic injury, LV pump function becomes depressed; cardiac output, stroke volume, BP, and compliance are reduced; and end systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end-diastolic pressure give rise to diastolic dysfunction.

Diagnosis

A patient is diagnosed with MI if two (probable) or three (definite) of the following criteria are satisfied:

  • Clinical history of ischemic-type chest pain lasting for more than 20 min
  • Changes in serial ECG tracings
  • Rise and fall of serum cardiac biomarkers such as CK-MB fraction and troponin.


Physical examination

The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38°C–39°C). BP may be elevated or decreased, and the pulse can become irregular.

If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and roles over the lung.[2] Electrocardiogram

The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. A serial ECG may be used to follow rapid changes in time. The standard 12 lead ECG does not directly examine the right ventricle and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. In particular, acute MI in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.[28]

Cardiac markers

Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. The markers most widely used in the detection of MI are serum glutamic-oxaloacetic transaminase, LDH, MB subtype of the enzyme creatine kinase and cTnT and cTnI. The cTnT and cTnI which are released within 4–6 h of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity. Heart-type fatty acid binding protein is another marker, used in some home test kits. Elevated troponins in the setting of chest pain may accurately predict a high likelihood of an MI in the near future. The diagnosis of MI requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-h period. Because these enzyme levels are not elevated immediately following a heart attack.[29]

Angiography

In difficult cases or in situ ations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (usually, the femoral artery) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter, and a sequence of X-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in interventional cardiology.[29]

Histopathology

Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, MI presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 h.[30]

Goal of treatment

  • Abort the infection
  • Salvage the area of jeopardized myocardium
  • Increase myocardial oxygen delivery
  • Decrease myocardial oxygen consumption
  • Provide symptomatic relief and reduce anxiety
  • Reduce mortality and improve quality of life.


Treatment

Allopathic treatment of myocardial infarction

The allopathic treatment includes supplemental oxygen, nitrates, pain control, beta blockers unfractionated heparin, fibrinolytics, angiotensin-converting enzyme (ACE) inhibitors, and glycoprotein IIb/IIIa, antagonists. The pharmacology of drugs is given in [Table 2].[31],[32],[33],[34],[35],[36],[37],[38]
Table 2: Allopathic treatment for myocardial infarction[31],[32],[33],[34],[35],[36],[37],[38]

Click here to view


Treatment outcomes

An individual patient's long-term outcome following an MI depends on numerous variables, some of which are not modifiable from a clinical standpoint. However, patients can modify other variables by complying with prescribed therapy and adopting lifestyle changes.

Stress testing

Cardiac stress testing after MI has established value in risk stratification and assessment of functional capacity. The degree of allowable physiologic stress during testing depends on the length of time from MI presentation. Stress testing is not recommended within several days after an MI. Only submaximal stress tests should be performed in stable patients 4–7 days after MI. Symptom-limited stress tests are recommended 14–21 days after an MI.[39]

Smoking cessation

Smoking is a major risk factor for coronary artery disease and MI. For patients, who have undergone an MI, smoking cessation is essential to recovery, long-term health, and prevention of reinfarction. All STEMI and NSTEMI patients with a history of smoking should be advised to quit and offered smoking cessation resources, including nicotine replacement therapy, pharmacologic therapy, and referral to behavioral counseling or support groups.[24]

Long-term medications

Most oral medications instituted in the hospital at the time of MI will be continued long term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACE inhibitors are continued indefinitely in patients with congestive heart failure, LV dysfunction, hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to diet modification, is continued indefinitely as well.[40]

Herbal treatment

Phytochemicals, which can suppress free radical generation and enhance endogenous antioxidant defense, may attenuate myocardial dysfunction during MI. Dietary antioxidants are considered beneficial because they slow down the chemical process of oxidation and repair the free radical damage which is implicated in the development of myocardial damage during MI.[41] The herbal plants with cardioprotective activity are shown in [Table 3].[42],[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54]
Table 3: Plants have cardioprotective activity[42],[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54]

Click here to view


The use of herbal medicines, one of the main therapeutic approaches of complementary and alternative medicine, can be traced back thousands of years ago in the East. Currently, there is a recent resurgence of the use of herbal medicines in popularity among patients in the West, and they were consumed by more than 15 million people in the US. With increasing enhancement of people's awareness of self-care and concerning on the inevitable adverse effects of conventional medicine, herbal medicines are favored by people with CVDs worldwide for their unique advantages in preventing and curing diseases, rehabilitation, and health care. There is growing evidence showing that many herbal medicines and their active ingredients contribute to the standard therapy for CVDs, for example, aspirin, digitalis, and reserpine.[55],[56],[57],[58]

In China, CHM is widely prescribed in both outpatient and inpatient settings.[59] Among community health clinics, 75% provide both BM and traditional Chinese medicine (TCM) treatments. TCM hospitals comprised 13.8% of all hospitals, and 90% of the BM hospitals are annexed with TCM departments.[60] Given the omnipresence of TCM services within the Chinese health-care system, it is not uncommon for clinicians to prescribe CHM as an adjunct to BM treatment in the management of potentially life-threatening conditions, including MI.[61] One of the most researched single herbs is Radix Astragali, which exerts its therapeutic effectiveness by inhibiting cardiac fibrosis, reducing infarct size, and increasing capillary and arteriole densities.[62] Commonly used Chinese proprietary medicines include Shexiang Baoxin tablets and Tongxinluo capsules. Shexiang Baoxin tablets are found to slow MI pathogenesis by inhibiting hypertrophy-related metabolites.[63] On the other hand, Tongxinluo capsules act by promoting local blood supply and thus limit infarct size.[64] CHM injections based on Sheng Mai San are also widely prescribed. It reduces infarct size through the activation of protein kinase C, opening of the mitochondrial KATP channels, and lowering the concentration of 5-hydroxytryptamine, norepinephrine, methionine-enkephalin, and leucine-enkephalin.[65],[66]

Recent updates on myocardial infarction diagnosis

The routine use of antiplatelet agents such as clopidogrel, prasugrel, or ticagrelor, in addition to aspirin, reduces patient morbidity and mortality. PCI in a timely manner is the primary treatment of patients with acute ST-segment elevation MI. Drug-eluting coronary stents are safe and beneficial with primary coronary intervention. Treatment with direct thrombin inhibitors during PCI is noninferior to unfractionated heparin and glycoprotein IIb/IIIa receptor antagonists and is associated with a significant reduction in bleeding. The intracoronary use of a glycoprotein IIb/IIIa antagonist can reduce infarct size. Pre- and post-conditioning techniques can provide additional cardioprotection.[67]

Ayurveda is a traditional and most commonly practiced form of medicine in India.[68] Ayurveda comes from the words Ayur (life) and Veda (knowledge). The concept of Ayurveda is based on a combined study of the body (Sharira), sense organs (Indriyas), mind (Manas), and soul (Atman).[69] Equilibrium of all these is related to health. When an imbalance exists among any one of the three Doshas, Ayurveda suggests a unique combination of food, exercise, meditation, and herbs. Ayurvedic herbs stimulate the function of specific organs in the body, possibly by altering hormones, affecting immunity and neurotransmitters, and conveying antioxidant properties.[70] Cardiovascular problems have been dealt in detail in Ayurveda, which describes Hridaya (heart) as a body organ governing emotions and circulating blood to keep a person alive and healthy. Heart disease (Hrudroga) is a global phenomenon. It is now becoming a major health problem even in developing countries.[71] The predisposing factors are heredity, high BP, diabetes, high serum cholesterol, and smoking. Improper diet and stressful lifestyles lead to thickening of arteries (Dhamani praticaya) or hardening of arteries (Dhamani kathinaya) resulting in angio-obstruction (Vata dosa) and angina (Ruja).[72]Kapha and pitta types are due to fat accumulations. Vata type is from the hardening of the arteries.[73],[74] The treatment for arteriosclerosis is similar to the treatment of heart diseases and for hypertension. Hypertension usually follows arteriosclerosis. Guggul lowers high cholesterol and is useful for Kapha. It improves circulation, reduces pain, removes accumulations, and promotes healing. One gram is taken in the morning and evening for 3 months. Garlic is taken along with honey. Calamus, turmeric, elecampane, aloe vera gel with turmeric or safflower, katuka, myrrh, saffron, motherwort, and hawthorn berries are other useful herbs.[74]

Recent advances

Thrombolytic drugs have reduced mortality in patients with acute MI, but current treatments have limited success in achieving immediate vessel patency and in maintaining this in the longer term. The best current thrombolytic treatment – accelerated tissue plasminogen activator – restores complete perfusion in only 54% of patients, while streptokinase achieves this in 30% only. Thrombolytic drugs such as recombinant plasminogen activator and prourokinase are being developed but must be tested in large clinical trials. The future of recently developed antithrombin drugs to reduce arterial re occlusion is uncertain. New platelet receptor blocking drugs seem to have the most potential to improve rates of immediate and long-term vessel patency. The greater benefits of primary angioplasty compared with thrombolytic have not been established definitively.[66] In an acute coronary syndrome, thrombus formation occurs under conditions of high shear stress and is principally driven by platelet aggregation. This dominance of platelet aggregation during intracoronary thrombus formation reflects the dramatic effects that antiplatelet therapies have on clinical outcomes. Aspirin was the first antiplatelet therapy which induced a halving in event rates in patients with acute coronary syndrome: such a large effect size has rarely been surpassed in other domains of cardiology. Given aspirin's remarkable success, it is perhaps unsurprising that adjunctive antiplatelet therapies have been investigated to build on these benefits, especially as there are multiple mechanisms of platelet activation beyond the cyclooxygenase pathway. However, as platelets are essential to primary hemostasis, there is a balance between reducing the incidence of future cardiovascular events and causing harm from an increased risk of bleeding. The P2Y12 receptor antagonists are a class of drugs that have gained widespread acceptance since they appear to provide additional thrombotic protection at the expense of modest increases in bleeding. Their use is principally associated with reductions in recurrent MI and in a few trials, reductions in cardiovascular events and mortality. Other anti-platelet therapies are available but have variable net clinical benefit and for the purposes of this review, we will consider only dual antiplatelet therapy with aspirin and P2Y12 receptor antagonism.[75],[76],[77],[78],[79]


  Myocardial Infarction and Influenza Infection Top


Jeffrey CK and team evaluated the association between laboratory-confirmed influenza infection and hospitalization for acute MI, whereas various high-specificity laboratory methods to confirm influenza infection in respiratory specimens and ascertained hospitalization for acute MI from the administrative data. They identified 364 hospitalizations for acute MI that occurred within 1 year before and 1 year after a positive test result for influenza and found that found a significant association between respiratory infections, especially influenza and acute MI.[80]


  Conclusion Top


Nowadays, it can be clearly seen that lifestyle of human beings is full of stress, pressure, and other normal health issues such as obesity, diabetes, and hypertension these health problems are responsible for the MI either directly or indirectly. A proper knowledge or guidance is the best solution of every problem. On behalf of this review, herbal drugs or formulations are found to be very good and safe. If research is specially focused on herbal plants, so it may be the best solution in future with low side effects.

Acknowledgment

I would like to express my hearty thanks to BBD University and Central Drug Research Institute, Lucknow for providing library facilities to access the journals and books.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Introduction
Physiology of Ca...
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Myocardial Infra...
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