Myocardial Infarction (Heart Attack): Complications

The following are the most important diseases or complications that may be contributed to by myocardial infarction (heart attack):

Endocrine, nutritional, and metabolic diseases (E00-E90).

  • Diabetes mellitus type 2

Cardiovascular system (I00-I99)

  • Acute cardiac death due to pump failure
  • Angina pectoris (“chest tightness”; sudden pain in the region of the heart) – myocardial infarction patients without relevant coronary stenoses (narrowing of the coronary arteries) are just as likely to suffer from angina pectoris after the heart attack as patients with coronary obstruction (occlusion of coronary arteries)
  • Apoplexy, ischemic* (stroke due to lack of blood flow due to vascular occlusion).
  • Blood pressure drop – most important symptoms of infarct-related cardiogenic shock (Ics) – but not obligatory – hypotension/low blood pressure < 90 mmHG systolic for at least 30 minutes, in association with signs of organ diminished perfusion/organ diminished perfusion: cold extremities, oliguria (decreased urine production with a daily maximum of 500 ml), mental changes such as agitation/sick restlessness
  • Bradycardia with AV blocks – drop in heart rate below 60/min. with conduction disturbance between atria and ventricles (20% of patients with acute coronary syndrome show AV block)
  • Dressler syndrome (synonyms: postmyocardial infarction syndrome, postcardiotomy syndrome) – pericarditis (inflammation of the pericardium) and/or pleurisy (inflammation of the pleura) occurring several weeks (1-6 weeks) after a myocardial infarction (heart attack) or injury to the myocardium (heart muscle) as a late immunologic reaction at the pericardium (heart sac) after formation of myocardial antibodies (HMA)
  • Embolism, arterial*
  • Heart failure (heart failure) (20-25% of cases): incidence (frequency of new cases) of de novo heart failure (new onset of heart failure) was significantly 34% higher in women than in men after acute ST-segment elevation myocardial infarction (STEMI) (25.1 vs 20.0%, odds ratio [OR] 1.34; 95% confidence interval [CI] 1.21-1.48).
    • Acute left heart failure (LHV) in left myocardial infarction due to LV ischemia (reduced blood flow to the left ventricle).
    • Acute right heart failure (RHV) in right myocardial infarction due to RV ischemia.
  • Cardiac arrhythmias – ventricular extrasystoles (cardiac actions occurring outside the normal heart rhythm); later also atrial fibrillation (VHF).
  • Cardiac wall aneurysm (circumscribed outpouching of the heart wall) with the formation of intracardiac thrombi (“blood sprouts in the heart”) and thromboembolic events (late complication).
  • Ventricular tachycardia – ventricular actions occurring outside the normal heart rhythm.
  • Ventricular fibrillation – life-threatening pulseless cardiac arrhythmia (Most common cause of death in the first few hours after myocardial infarction).
  • Cardiogenic embolism – heart-related occlusion of a vessel by a thrombus (blood clot), especially by atrial fibrillation.
  • Cardiomyopathy, ischemic – heart muscle disease with narrowed or occluded coronary arteries (late complication).
  • Mitral valve regurgitation – inability of the mitral valve to close.
  • Papillary muscle rupture (rupture of the papillary muscles located on the inner wall of the heart chambers) with acute mitral valve regurgitation (late complication)
  • Pericarditis (inflammation of the pericardium) or postinfarction pericarditis (late complication).
  • Sudden cardiac death (PHT)
  • Reinfarction – renewed myocardial infarction
  • Wall rupture with pericardial tamponade – wall rupture with bleeding into the pericardium.

* Myocardial patients receiving nonsteroidal anti-inflammatory drugs (NSAIDs) in combination with antithrombotic therapy (= anticoagulant therapy), regardless of whether the drug was a selective or nonselective COX-2 inhibitor, had a twofold risk of bleeding compared with patients who had not taken an additional NSAID. The secondary end point, consisting of cardiovascular death, repeat myocardial infarction, TIA, ischemic apoplexy, or arterial embolism, also reflected the negative impact of NSAID use (observation period: 3.5 years). Psyche-Nervous System (F00-F99; G00-G99).

  • Erectile dysfunction (ED; erectile dysfunction).
  • Transient ischemic attack* (TIA) – sudden onset of circulatory disturbance in the brain leading to neurologic dysfunction that resolves within 24 hours
  • Female sexual dysfunction: As a cause of sexual inactivity after myocardial infarction, 40% of women reported a lack of interest and 22% reported vaginal dryness.

Symptoms and abnormal clinical and laboratory findings not elsewhere classified (R00-R99).

  • Cardiogenic shock (form of shock caused by weakened pumping action of the heart)-approximately 90% of patients survive a myocardial infarction; if cardiogenic shock occurs initially or during the course of a myocardial infarction, the survival rate of infarct-related cardiogenic shock (ICS) patients is only approx. 50%, due toformation of a multiorgandysfunction syndrome (MODS)/simultaneous or sequential failure or the severe functional impairment of various vital organ systems of the body.
  • Noncardiac chest pain (chest pain)-occurring in 29% of patients hospitalized with chest pain within 1 year of myocardial infarction; their quality of life is just as poor in those readmitted with angina.

Further

  • Neuroinflammation (inflammatory response in the brain); detection was by positron emission tomography (PET).
  • Elective surgery (surgery that is not really urgent (elective surgery) or surgery whose timing can be chosen almost freely) during the first 60 days after a myocardial infarction is associated with a higher risk of complications:
    • Re-infarction rate (recurrence of infarction): 32.8% by postoperative day 30; mortality rate (death rate): 14.2% (patients without prior infarction: 30-day infarction rate 1.4%; mortality rate 3.9%).
    • Re-infarction rate: 8.4% in days 61-90; mortality rate: 10.5%.

Prognostic factors

  • The mortality (death rate) of patients with acute coronary syndrome (ACS) aged >75 years is markedly increased compared with younger patients.
  • Diet
    • Patients with ST-segment elevation myocardial infarction (STEMI) who eat dinner just before bedtime and skip breakfast in the morning have a worse prognosis after myocardial infarction: within 30 days of hospital discharge, they had a four- to fivefold higher risk of dying or having another heart attack or angina.
    • Dietary intake of omega-3 fatty acids (omega-3 FAs): the higher the dietary intake of omega-3 fatty acids measurable in the blood, the lower the rate of rehospitalization for cardiovascular complications and the mortality rate (death rate). This was true both for eicosapentaeinic acid (EPA) consumed mainly by fish and for alpha-linolenic acid (ALA), an omega-3 fatty acid of plant origin.
  • Patients with underweight (BMI < 18.5 kg/m2) had a higher mortality risk after myocardial infarction than patients with a BMI in the normal range (18.5-24.9 kg/m2): the adjusted mortality risk (risk of death) was up to 27% higher; in the high-normal range from 24 kg/m2 upwards, the mortality risk was lowest (subjects: 57,574 infarction patients; underweight: 5,678; follow-up: 17 years).
  • Five years after myocardial infarction, lethality was highest in underweight patients with a BMI of <22 (plus 41%) and lowest in myocardial infarction survivors with a BMI between 25 and 35.
  • Patients with severe obesity (BMI greater than 35) also had a significantly increased 5-year mortality/sterility rate (plus 65 percent), as did patients with android fat distribution (visceral fat) [abdominal circumference >100 cm in women or greater than 115 cm in men].
  • Chronic cannabis use: with continued use, a dose-dependent increase in risk of mortality (mortality) has been demonstrated for patients after myocardial infarction.
  • Heart rates (I: < 50; II: 50-69; III: 70-89; IV: ≥ 90/min) on hospital admission:
    • Group I: patients had already suffered myocardial infarction more frequently; overall survival at 3 months was significantly worse than in group IV.
    • Group IV: Patients admitted to a specialized CPU (chest pain unit) had worse survival at 3 months despite an optimal treatment environment.
  • Blood pressure at hospital admission is inversely (inversely) associated with long-term mortality (death rate) after acute myocardial infarction, ie, the higher the blood pressure the lower the mortality. Low blood pressure on admission should be understood as a warning sign in these patients.
  • Resting heart rate increased at hospital discharge (in patients with left ventricular dysfunction); the lowest 1-year mortality of 6.7% was in the quartile with the lowest heart rate (<60 per minute), in the 2nd quartile (<60 per minute), and in the 3rd quartile (<60 per minute). Quartile (61-62 per minute) mortality was 7.7% in the 3rd quartile (68-75 per minute), and in the highest quartile mortality increased to 13.2%; 5-year mortality for these groups was 20.0%, 23.1%, 45.7%, and 30.3%, respectively.
  • Patients with anxiety disorders and incident myocardial infarction, responded more quickly and arrived at the emergency department two hours earlier.
  • Stress may impede recovery from myocardial infarction in younger patients. Women were more likely than men to report psychosocial stressful experiences. Overall, this had a negative effect on recovery in both sexes.
  • Acute coronary syndrome (AKS; acute coronary syndrome, ACS):
    • Optimism led to better recovery from acute coronary syndrome and significantly reduced the risk of hospital readmission for coronary disease by 8%.
    • Iron deficiency increases the risk of cardiovascular death or nonfatal myocardial infarction by 70% within four years compared with patients without iron deficiency
  • The predictive value of left bundle branch block (LSB) for the diagnosis of acute transmural (“affecting all layers of an organ wall”) myocardial infarction (AMI) was very low (sensitivity of 38% and positive predictive value of 58%). The prevalence (disease frequency) of cardiovascular risk factors and end-organ damage in LSB was increased compared with patients with ST elevation, and there was also more frequent pulmonary edema or cardiogenic shock.In the study, AMI was confirmed in 58.3% of patients with LSB and in 86.4% with ST elevation. A new-onset LSB in acute chest pain (chest pain) characterizes a patient population with high morbidity (disease incidence) and mortality (death rate).
  • Postinfarction mortality is greatly increased in patients with severe mental illness. Overall 30-day mortality was 10 percent. Bipolar patients had an increased mortality (death rate) of about 38 percent, and schizophrenia patients had an increased mortality (death rate) of about 168 percent.
  • Diabetes mellitus: according to adjusted analysis, diabetes was an independent risk factor in
    • ST-segment-elevation myocardial infarction (STEMI; English : ST-segment-elevation myocardial infarction): increased mortality risk (risk of death) by 56
    • Non-ST-segment-elevation myocardial infarction (NSTEMI; engl. : non ST-segment-elevation myocardial infarction): 39% increased mortality risk.

    compared to infarction patients without diabetes

  • Latent hypothyroidism (subclinical hypothyroidism/thyroid insufficiency): 3-fold higher cardiovascular mortality (death rate) in patients with an acute coronary event compared with normal thyroid function. Substitution therapy with levothyroxine for 52 weeks did not result in greater improvement in left ventricular ejection fraction (LVEF; EF) than placebo therapy.
  • Increased mortality (death rate) with hyperkalemia (excess potassium):
    • Increased 13.4% if a value of at least 5.0 mEq/l was measured only once
    • 16.2% increased when hyperkalemia was measured twice
    • 19.8% elevated when a value of at least 5.0 mEq/l was reached at least three times
  • Medications:

GRACE score

  • The Global Registry of Acute Coronary Events (GRACE) score is a prognostic calculation tool for the first six months following a coronary event.The following information is evaluated: Age, heart rate, systolic blood pressure, presence of heart failure (cardiac insufficiency), renal insufficiency (renal weakness), creatinine level, ST-segment deviation, any cardiac arrest suffered, troponin elevation and diuretic prescriptions.The calculation is Internet-based: [literature: see below of the internet site]. Interpretation of values:
    • ≤ 88 indicates low risk (post-hospital mortality (death rate) <3%).
    • > 118 represents a high risk (mortality rate > 8 %)

Risk score used to calculate the probability of a major cardiovascular event (MACE) in the year after a myocardial infarction.

Major cardiovascular event (MACE) is defined as recurrence of myocardial infarction (heart attack), apoplexy (stroke), heart failure, or death.

Risk factor Points
Age:
– 64-75 years 6
– 75-84 years 9
– ≥ 85 years 14
No university degree 4
No medical care before emergency room 3
Previous angina pectoris (chest tightness, heart pain) 5
Previous myocardial infarction 4
History of ventricular tachycardia/fibrillation 6
Hypertension (high blood pressure) 2
Symptoms > 4 hrs before admission 3
Renal dysfunction (serum creatinine > 2.5 mg/dl) 4
Ejection fraction (ejection fraction):
– – < 40 % 8
– not measured 6
Leukocyte count (white blood cell count):
– 6,000-12,000/µl 4
– > 12,000/µl 7
Fasting glucose (fasting blood glucose) > 216 mg/dl 5
Resting heart rate > 90/min 5
Systolic blood pressure <100 mmHg 4
Any complication in hospital 2

Interpretation

  • 0-10 points: low risk [1% in the first year].
  • 11-30 points: medium risk [6% in the first year].
  • ≥ 31 points: high risk [32% in the first year].

Further notes

  • Abdominal obesity (men: waist circumference > 102 cm or women: 88 cm) is a prognostic factor after myocardial infarction for further atherosclerotic cardiovascular events (ASCVD), ie, nonfatal myocardial infarction, CHD-related death, or stroke.