What is Myocardial Infarction?

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OpenStax Anatomy and Physiology

Myocardial infarction (MI) is the formal term for what is commonly referred to as a heart attack. It normally results from a lack of blood flow (ischemia) and oxygen (hypoxia) to a region of the heart, resulting in death of the cardiac muscle cells. An MI often occurs when a coronary artery is blocked by the buildup of atherosclerotic plaque consisting of lipids, cholesterol and fatty acids, and white blood cells, primarily macrophages. It can also occur when a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the smaller vessels. The resulting blockage restricts the flow of blood and oxygen to the myocardium and causes death of the tissue. MIs may be triggered by excessive exercise, in which the partially occluded artery is no longer able to pump sufficient quantities of blood, or severe stress, which may induce spasm of the smooth muscle in the walls of the vessel.

In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris, often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpations), nausea and vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple indigestion, so differential diagnosis is critical. It is estimated that between 22 and 64 percent of MIs present without any symptoms.

An MI can be confirmed by examining the patient’s ECG, which frequently reveals alterations in the ST and Q components. Some classification schemes of MI are referred to as ST-elevated MI (STEMI) and non-elevated MI (nonSTEMI). In addition, echocardiography or cardiac magnetic resonance imaging may be employed. Common blood tests indicating an MI include elevated levels of creatine kinase MB (an enzyme that catalyzes the conversion of creatine to phosphocreatine, consuming ATP) and cardiac troponin (the regulatory protein for muscle contraction), both of which are released by damaged cardiac muscle cells.

Immediate treatments for MI are essential and include administering supplemental oxygen, aspirin that helps to break up clots, and nitroglycerine administered sublingually (under the tongue) to facilitate its absorption. Despite its unquestioned success in treatments and use since the 1880s, the mechanism of nitroglycerine is still incompletely understood but is believed to involve the release of nitric oxide, a known vasodilator, and endothelium-derived releasing factor, which also relaxes the smooth muscle in the tunica media of coronary vessels. Longer-term treatments include injections of thrombolytic agents such as streptokinase that dissolve the clot, the anticoagulant heparin, balloon angioplasty and stents to open blocked vessels, and bypass surgery to allow blood to pass around the site of blockage. If the damage is extensive, coronary replacement with a donor heart or coronary assist device, a sophisticated mechanical device that supplements the pumping activity of the heart, may be employed. Despite the attention, development of artificial hearts to augment the severely limited supply of heart donors has proven less than satisfactory but will likely improve in the future.

MIs may trigger cardiac arrest, but the two are not synonymous. Important risk factors for MI include cardiovascular disease, age, smoking, high blood levels of the low-density lipoprotein (LDL, often referred to as “bad” cholesterol), low levels of high-density lipoprotein (HDL, or “good” cholesterol), hypertension, diabetes mellitus, obesity, lack of physical exercise, chronic kidney disease, excessive alcohol consumption, and use of illegal drugs.

Source:

Betts, J. G., Young, K. A., Wise, J. A., Johnson, E., Poe, B., Kruse, D. H., … DeSaix, P. (n.d.). Anatomy and Physiology. Houston, Texas: OpenStax. Access for free at: https://openstax.org/details/books/anatomy-and-physiology

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BRG1 protects the heart from acute myocardial infarction by reducing oxidative damage through the activation of the NRF2/HO1 signaling pathway

Brahma-related gene 1 (BRG1) regulates the chromatin structure and expression of cardiac genes. Although BRG1 is downregulated in adult cardiomyocytes, it is reactivated during cardiac stress. The role of BRG1 in acute myocardial infarction (AMI) has not been clearly defined. This study assessed the protective role of BRG1 in AMI using cell cultures and an animal model and explored the underlying molecular events. The results showed that in the peri-infarct zone, expression of BRG1 protein was significantly increased relative to the sham group, which was accompanied by NRF2 and HO1 upregulation and KEAP1 downregulation. BRG1 overexpression through adenoviral intramyocardial injection into AMI mice reduced the infarct size and improved cardiac functions with upregulation of NRF2 and its target HO1 and attenuated oxidative damage and cell apoptosis. However, shRNA-mediated Brg1 knockdown had the opposite effects. These results were further confirmed in cultured primary neonatal rat cardiomyocytes (NRCMs) with oxygen-glucose deprivation (OGD). Moreover, the selective NRF2 inhibitor brusatol could partially reverse cardiomyocyte antioxidant ability and BRG1 overexpression-induced cardiac protection in vitro. In addition, co-immunoprecipitation and immunofluorescence data showed that BRG1 overexpression significantly promoted the BRG1/NRF2 co-localization in cardiomyocytes. The chromatin immunoprecipitation-qPCR revealed BRG1 interaction with the Ho1 promoter and BRG1 overexpression could induce BRG1 binding to the Ho1 promoter during the OGD. In conclusion, this study demonstrated that BRG1 upregulation during AMI in vitro and in vivo increased the NRF2 level and NRF2 nuclear accumulation for HO1 expression to alleviate cardiac myocyte oxidative stress and upregulate cardiomyocyte viability. The BRG1-NRF2-HO1 pathway may represent a novel therapeutic target in the prevention of cardiac dysfunction in AMI patients.

Keywords: Brahma-related gene 1; Myocardial infarction; Nuclear factor erythroid 2-related factor 2; heme oxygenase-1; oxidative damage.

https://pubmed.ncbi.nlm.nih.gov/32950688/

Hospital admissions for acute myocardial infarction before and after lockdown according to regional prevalence of COVID-19 and patient profile in France: a registry study

Background: The COVID-19 pandemic has had a profound effect on general health care. We aimed to evaluate the effect of a nationwide lockdown in France on admissions to hospital for acute myocardial infarction, by patient characteristics and regional prevalence of the pandemic.

Methods: In this registry study, we collected data from 21 centres participating in the ongoing French Cohort of Myocardial Infarction Evaluation (FRENCHIE) registry, which collects data from all patients admitted for ST segment elevation myocardial infarction (STEMI) or non-ST segment elevation myocardial infarction (NSTEMI) within 48 h of symptom onset. We analysed weekly hospital admissions over 8 weeks: the 4 weeks preceding the institution of the lockdown and the 4 weeks following lockdown. The primary outcome was the change in the number of hospital admissions for all types of acute myocardial infarction, NSTEMI, and STEMI between the 4 weeks before lockdown and the 4 weeks after lockdown. Comparisons between categorical variables were made using χ2 tests or Fisher’s exact tests. Comparisons of continuous variables were made using Student’s t tests or Mann-Whitney tests. Poisson regression was used to determine the significance of change in hospital admissions over the two periods, after verifying the absence of overdispersion. Age category, region, and type of acute myocardial infarction (STEMI or NSTEMI) were used as covariables. The FRENCHIE cohort is registered with ClinicalTrials.gov, NCT04050956.

Findings: Between Feb 17 and April 12, 2020, 1167 patients were consecutively admitted within 48 h of acute myocardial infarction (583 with STEMI, 584 with NSTEMI) and were included in the study. Admissions for acute myocardial infarction decreased between the periods before and after lockdown was instituted, from 686 before to 481 after lockdown (30% decrease; incidence rate ratio 0·69 [95% CI 0·51-0·70]). Admissions for STEMI decreased from 331 to 252 (24%; 0·72 [0·62-0·85]), and admissions for NSTEMI decreased from 355 to 229 (35%; 0·64 [0·55-0·76]) following institution of the lockdown, with similar trends according to sex, risk factors, and regional prevalence of hospital admissions for COVID-19.

Interpretation: A marked decrease in hospital admissions was observed following the lockdown, irrespective of patient characteristics and regional prevalence of COVID-19. Health authorities should be aware of these findings, in order to adapt their message if the COVID-19 pandemic persists or recurs, or in case of future major epidemics.

Funding: Recherche Hospitalo-Universitaire en Santé iVasc.

https://pubmed.ncbi.nlm.nih.gov/32950075/

Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA)

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is the current term used to describe patients who have a myocardial infarction but have normal, non-obstructed coronary arteries on a coronary angiogram. There is still much debate over the definition, diagnosis, management and treatment of MINOCA. However, MINOCA is not a benign condition; prompt recognition and diagnosis can lead to better management and treatment and thus improve patient outcomes. This review article will update the most recent definition of MINOCA, discuss epidemiology and etiology, and review the diagnostic workup and management options for patients presenting with signs and symptoms of MINOCA.

https://pubmed.ncbi.nlm.nih.gov/32947482/

Chest Pain Severity Rating Is a Poor Predictive Tool in the Diagnosis of ST-Segment Elevation Myocardial Infarction

Current ST-segment elevation myocardial infarction (STEMI) guidelines require persistent electrocardiogram (ECG) ST-segment elevation, cardiac enzyme changes, and symptoms of myocardial ischemia. Chest pain is the determinant symptom, often measured using an 11-point scale (0-10). Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. This retrospective observational cohort study considered consecutive STEMI patients from 5/02/2009-12/31/2018. Analysis of standard STEMI metrics included positive ECG-to-device and first medical contact (FMC)-to-device times, presence of comorbidities, false positive diagnosis, 30-day and 1-year mortality, and 30-day readmission. Chest pain severity was assessed upon admission to the primary percutaneous coronary intervention (PPCI) hospital. We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7 years). Of these, 251 (17.8%) had no obstructive lesion, consistent with false positive STEMI. 466 (33.1%) reported chest pain rating of 0 on admission, 378 (26.8%) reported mild pain (1-3), 300 (21.3%) moderate (4-6), and 265 (18.8%) severe (7-10). Patients presenting without chest pain had a significantly higher rate of false positive STEMI diagnosis. Increasing chest pain severity was associated with decreased time from FMC to device, and decreased in-hospital, 30-day and 1-year mortality. Severity of chest pain on admission did not correlate to the likelihood of a true positive STEMI diagnosis, although it was associated with improved patient prognosis, in the form of improved outcomes, and shorter times to reperfusion.

https://pubmed.ncbi.nlm.nih.gov/32947377/

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