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Myocardial infarction

See ((Acute myocardial infarction (AMI) ))

Approximately 1.3 million Americans sustain a myocardial infarction annually.

Almost half of heart attacks and sudden deaths occur without prior symptoms.

Coronary angiography studies show half of culprit lesions that cause acute myocardial infarction are insufficiently stenotic to be flow limiting prior to plaque rupture, this limiting the utility of noninvasive ischemic-based strategies.

The pathophysiology basis is that coronary plaque ruptures that precipitate myocardial infarction are not necessarily stenotic, and stenotic plaques are not necessarily vulnerable.

In 2008 there was approximately 8,000,000 US adults who survived a myocardial infarction(Roger VL et al).

Proportion of cases that myocardial infarction occurring in young patients varies between two and 10% in the past few decades.

Approximately 5-10% of all patients diagnosed with myocardial infarction do not have significant coronary stenosis, referred to as nonobstructive coronary arteries.

Nonobstructive coronary artery disease leading to myocardial infarction may be the result of plaque disruption, spasm, thromboembolism, dissection, microvascular dissection, myocardial injury due to supply/demand mismatch, nondetected myocarditis, or takotsubo syndrome.

Types of Myocardial Infarction

Type 1: Ischemic myocardial necrosis due to plaque rupture (ACS)

 

Type 2: Ischemic myocardial necrosis due to supply-demand mismatch, e.g. coronary spasm, embolism, low or high blood pressures, anemia, or arrhythmias.

 

Type 3: Sudden cardiac death 

 

Type 4: Procedure related, post PCI or stent thrombosis 

 

Type 5: Post CABG 

Type I MI is the result of atherosclerotic coronary artery disease with thrombotic coronary arterial obstruction secondary to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection.

Type I Plaque rupture or erosion leads to activation of the clotting cascade resulting in coronary arterial thrombosis, myocardial ischemia, and myocyte necrosis.

Type one myocardial infarction patients can have ST elevation or non-ST elevation myocardial infarction and are usually treated with medication and stenting of the culprit lesion in the coronary artery.

Type 2 MI patients do not have atherosclerotic plaque rupture but myocardial necrosis secondary to increased myocardial oxygen demand or decreasing myocardial blood flow.

Type 2 MI categorized as a myocardial infarction secondary to an ischemic imbalance between blood supply and myocardial oxygen demand.

With Type 2 MI patients may or may not have atherosclerotic disease.

Type 2 myocardial infarction is also the result of ischemic myocardial necrosis, but not from plaque rupture or erosion but with subsequent coronary arterial thrombosis.

Type 2 MI may occur in the patient with hypotension or a tachyarrhythmia: The delivery of oxygen and nutrients to the myocardium are inadequate because of increased metabolic demand from the tachycardia.

A similar occurrence for Type 2 myocardial infarction would be a gastrointestinal hemorrhage and secondary hypotension  that decreases the delivery of oxygen and nutrients to the myocardium, resulting in myocyte ischemia and necrosis.

Myocardial ischemic injury with necrosis resulting in the in balance between myocardial oxygen supply or demand occurs with coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachyarrhythmias, bradyarrhythmias, anemia, respiratory failure, hypotension, and hypertension with the without left ventricular hypertrophy leading to myocardial infarction type 2.

Type 1 MI makes up about 70+ percent of patients with MI and 26% or so have Type 2 disease.

In Type 1 MI only 12% of patients have normal coronary angiograms.

Type 2 patients more likely to be older, female and have lower blood troponin values and have more comorbidities.

In type 2 MI approximately 50% of patients have normal coronary angiogram.

In type 2 Mi mortality rate is high, reaching approximately 50% after two years (Saaby L et al ).

Patients with type 2 myocardial infarction are less likely to undergo coronary revascularization or to be treated with dual antiplatelet therapy, statins and beta blockers in patients with type 1 myocardial infarction.

The excess mortality in type 2 myocardial infarction is more likely caused by the nature of myocardial infarction rather than patient comorbidities.

Type 2 MI associated with anemia, renal failure, chronic obstructive pulmonary disease, and heart failure.

Type 3 MI is the result of coronary arterial thrombosis with early death.

Type 4 MI and type 5 MI relate to complications of percutaneous coronary intervention and coronary bypass surgery.

Management of patients with Type 1 and Type 2  myocardial infarction are different, with type 1MI, the goal is to restore myocardial blood flow while reducing myocardial metabolic demand. 

Therapy for type 2MI has  not been established, but suggests that correction of the entity that led to the imbalance between supply and demand should be the primary approach.

Type 1 myocardial infarctions tend to be larger than type 2 MIs based on peak blood troponin level.

Type 2 Myocardial infarction patients are commonly older, female patients with comorbidities. 

Type2 myocardial infarction patients usually demonstrate unremarkable non-specific findings on the EKG. 

Type 1 myocardial infarction patients are usually first seen in the emergency department with chest pain, and ischemic changes on EKG.

Each year an estimated 785,000 patients will have a new MI, and approximately 470,000 will have a recurrentv MI (Roger VL et al).

People with non-O blood groups-A,B, AB have a greater risk for heart attacks.

Approximately one of every 7 people with acute myocardial infarction wii die of its consequences.

One quarter to one half had a myocardial infarction with ST-segment elevation.

ST-segment elevation myocardial infarction (STEMI) is a subset of myocardial infarction with characteristic symptoms of myocardial ischemia, ST segment elevation or new or presumed new left bundle branch block.

Approximately 29% of patients with MI present with STEMI.

25-35% will die before receiving medical attention, most from ventricular fibrillation.

MIs more commonly originate in the LAD, left circumflex, and right coronary arteries and that over half of these MIs originate in the proximal portion of these vessels. 

 

The hot spots for prophylactic stenting would thus be within the first 20 mm of both the left anterior descending and left circumflex arteries and between 15 mm and 40 mm in the right coronary artery.

Associated with 25% mortality rate at 3 years.

Women are generally older than men at the time of hospitalization for myocardial infarction.

In-hospital mortality 11.2% in 1990 and fell to 9.4% in 1999 due to decreased mortality among patients with ST-segment elevation as a result of improvement in initial therapy with fibrinolysis or percutaneous intervention.

National Registry of Myocardial Infarction indicates that in hospital mortality was 5.7% among patients receiving reperfusion therapy compared with 14.8% among those eligible for similar therapy but did not receive such.

Associated with diabetes results in three-fold increase in mortality.

Smokers are 3 times more likely to have an MI, and persistent smoking after an acute MI carries a 50% higher chance of death in the firts two years.

Typical symptoms is chest discomfort, with sensation of pain or pressure over the middle or left side of the chest.

Many patients have neck pain, arm or shoulder pain, usually on the left side.

Some patients experience pain in the upper abdomen.

Unusual presentations include nausea or feeling of fullness in the upper abdomen, sweating or dyspnea.

Typical symptoms occur in about half of patients and occur more often in men than woman.

Large numbers of patients with myocardial infarction lack chest pain or chest discomfort at presentation.

Patients without chest pain or chest discomfort presented later, are treated less aggressively, and have almost twice the short-term mortality compared with patients presenting with more typical symptoms.

Younger women with myocardial infarction have a higher mortality risk than men, and the lack of chest pain or chest discomfort may contribute to that risk to that risk.

Women hospitalized with myocardial infarction are more likely present without chest pain or chest discomfort, and have a higher mortality than men within the same age group, but sex differences in clinical presentation without chest pain and in mortality are attenuated with increasing age (Canto JG et al).

Within 5 years after a first myocardial infarction, at 45-64 years of age, death occurs in 11% of white males, 16% of African American males, 17% of white females and 28% of African American females (Benjamin EJ).

Study: A total of 6,720,639 weighted hospitalizations for MI (79.8% NSTEMI, and 20.2% STEMI) were included in a study: The incidence rate of hospitalizations for MI was lower in women than men across all age groups. 

Women were less likely than men to undergo coronary angiography, revascularization, or to use circulatory-support devices. 

These differences were consistent across all age groups.

Compared with men, women have lower incidence of MI and less likelihood of undergoing invasive treatment regardless of age.

The negative impact of female sex on most outcomes was most pronounced in young and middle-aged women.

As a consequence of MI normal contractile tissue is replaced by noncontracttile fibrosis i.e. scar.

Cardiovascular magnetic resonance is the standard test to define the presence of myocardial scar.

Patients with diabetes often experience little symptoms despite having a significant process.

Myocardial infarction can be misdiagnosed by misinterpretation of electrocardiograms and 23-40% of misdiagnosed cases.

Misdiagnosis more common in younger patients, in less experienced physicians, and atypical presentations.

Often patients experience fatigue in the days prior to the event.

Progressive angina may occur prior to the event.

Anterior, inferior, and lateral infarctions classically attributed to occlusions of the left anterior descending artery, right coronary artery and left circumflex artery, respectively.

Right ventricle infarction carries the worst prognosis of any territorial subtype of MI (Assali AR et al).

Right ventricular infarction has a mortality of 10% by 30 days.

Approximately 6 1/2% of patients with acute MI present was left bundle branch block.

Chest pain may not be present in up to half of patients with LBBB and acute MI (Shipak MG).

Occur with disproportionate frequency early in the morning, around the time of wakening.

Plaque disruption with exposure of tissue factor to blood coagulation factors is a major cause of thrombosis.

More than 75% of major coronary thrombotic events are precipitated by atherosclerotic plaque rupture that exposed subendothelial plaque constituents to the blood stream.

The seven most important variables in predicting prognosis are age, cardiac arrest, anterior or lateral location of infarct, systolic blood pressure, serum creatinine, congestive heart failure and WBC count.

Strong independent association between increasing WBC count and 30-day mortality.

Increased WBC increases the risk of developing a first acute myocardial infarction.

Age follows a nonlinear relationship with mortality with a 30% 30- day mortality for patients >85 years and 9.5% for patients 65-74 years.

Elderly patients with myocardial infarction and reduced ventricular function have substantial morbidity and mortality in the first year after hospital discharge.

More than one-third of elderly patients with left ventricular ejection fraction less than 40% who survived hospitalization die within 1 year.

Left ventricular ejection fraction is an independent risk factor for sudden death after an myocardial infarction and is the basis for determining eligibility for ICD therapy.

The risk of death increases markedly if the left ejection fraction is 40% or less.

More than half of all myocardial infarctions occur in persons with less than 50% stenosis in the involved coronary artery.

In the year after a MI the subsequent rate of mortality is 10 %.

Best predictors of mortality within 30 days include advanced age, female sex, increased heart rate, lower systolic blood pressure, severity of prior angina, ST-segment depression and signs of heart failure.

Survivors have a mortality rate of 3-14 times that of the general population.

Perioperative stress precipitates myocardial infarction in patients with chronic flow-limiting coronary stenosis.

The majority of acute myocardial infarctions are not associated with Q-waves.

WBC count greater than 10,000 cells/dL associated with increased risk of mortality.

The resting heart rate measured at the time of hospital admission for a patient with acute myocardial infarction predicts mortality.

The heart rate measured on admission is dependant on sympathetic activity.

Elevated heart rate during hospital stay associated with an increased risk of death.

Elevated heart rate during the first year after myocardial infarction predicts for long term all-cause and cardiovascular mortality.

Depression three times more common after myocardial than in the general community, and its presence increases the risk of CV events and mortality.

Use of antipsychotic medications is associated with a modest increase in the risk of MI among community dwelling older patients with treated dementia.

The increased risk of myocardial infarction occurs at the beginning of treatment with anti-psychotic agents in patients with elderly who have dementia.

A significant portion of the racial and ethnic disparity in time to reperfusion treatment is accounted for by the hospital to which a patient is admitted in contrast to differential treatment inside the hospital.

For the first 6-12 months after an myocardial infarction patients are at high risk of death from arrhythmia.

Os may form after myocardial infarction that may lead to intramyocardial reentry arrhythmias resulting in ventricular tachycardia and may precipitate cardiac arrest in the absence of active ischemia.

Ventricular tachycardia may develop days or years after infarction.

Remodeling of ventricle after an infarct can lead to heart failure which can lead the ventricular tachycardia and sudden death.

Angiotensin converting enzyme inhibitors attenuate left ventricular remodeling, in part by reducing vascular load, and reduce morbidity and mortality.

In patients with left ventricular dysfunction and increased vascular load relative to ventricular contractility results in decreased myocardial efficiency.

Increased ventricular load contributes to dilatation of he left ventricle and ultimately to a poor prognosis.

Absolute risk of sudden death after myocardial infarction is highest in the first year.

Highest risk of sudden death after myocardial infarction is the first month with an event rate of 1.4% and subsequent rate of 0.14 to 0.18% per month thereafter.

The greatest risk of sudden death is the first week after a myocardial infarction and falls rapidly during the first month.

 

 

 

After first myocardial infarction, there is an inverse association between frequency of sexual activity and mortality.

Mechanical complications after myocardial infarction include rupture of the ventricular wall and rupture of the papillary muscle.

Mechanical complications occur most often in the first week following myocardial infarction.

Risk factors for myocardial infarction complications include a history of first myocardial infarction without angina, advanced age, female gender, hypertension, delayed diagnosis of myocardial infarction and prolonged physical activity during the event.Youdiagnosis, speed the diagnosis and implement treatment.

LateTIME trial of intracoronary infusion of autologous bone marrow mononuclear cells 2-3 weeks after MI with percutaneous coronary intervention did not improve global or regional ventricular function at 6 months compared to placebo.

In a randomized trial of chelation with disodium EDTA vs placebo in stable patients with prior MI, chelation therapy modestly reduced risk of adverse cardiovascular outcomes, many of which were revascularization procedures: conclusion- findings do not support routine use in patients with a prior MI (Lamas GA et al, TACT randomized trial).

Colchicine Cardiovascular Outcomes Trial (COLCOT) utilized at a dose of 0.5 mg daily in patients with recent myocardial infarction lead to a significantly lower risk of ischemic cardiovascular events than placebo: supporting the role of inflammation in atherosclerosis and its complications.

Scar tissue following a myocardial infarction is composed primarily of collagen and strengthened with cross-linked fibers that does not contract as well as healthy muscle tissue, and can compromise the organs ability to pump blood and lead to heart failure, arrhythmias, and sudden cardiac death.

 

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