Cardiovascular disease
Sally Robinson in Priorities for Health Promotion and Public Health, 2021
A heart attack, also called a myocardial infarction, occurs because the blood supply to the heart muscle, travelling in the coronary arteries, has been cut off, causing some heart tissue to die. The symptoms of a heart attack are discomfort or pain in the chest that does not go awaymild to severe pain that spreads to the arms, neck, jaw, stomach or backnausea, sweating, feeling short of breath and light-headednone or only some of the above
The heart, lungs and pleura
Kevin G Burnand, John Black, Steven A Corbett, William EG Thomas, Norman L Browse in Browse’s Introduction to the Symptoms & Signs of Surgical Disease, 2014
Complications of myocardial infarction may produce additional signs: A gallop rhythm indicates left ventricular failure.Ischaemic rupture of the chordae tendineae will result in acute mitral regurgitation and a pansystolic murmur.Postinfarct VSD causes a harsh systolic murmur, loudest at the lower left sternal edge.Some patients who survive a large full-thickness infarct may develop a left ventricular aneurysm. This may lead to heart failure, and arrhythmias.
Cardiac Disease 1
Len Sperry in Behavioral Health, 2013
Some of the more common heart diseases and conditions are briefly described. Coronary artery disease occurs when coronary arteries, the vessels that supply blood to heart muscle, become hardened and narrowed due to the buildup of cholesterol and other material, called plaque, on their inner walls. As the plaque increases in size, the inner surfaces of the coronary arteries get narrower and less blood can flow through them. Eventually, blood flow to the heart muscle is reduced, and, because blood carries much-needed oxygen, the heart muscle is not able to receive the amount of oxygen it needs. Reduced or cutoff blood flow and oxygen supply to the heart muscle can result in angina; that is, chest pain or discomfort that occurs when the heart receives an insufficient supply of blood. It is a symptom of coronary artery disease rather than a separate disease entity. Heart failure, commonly referred to as congestive heart failure, is a condition of ineffective heart pumping such that vital organs get insufficient blood, resulting in such signs and symptoms as shortness of breath, fluid retention, and fatigue. It results when heart failure has led to fluid buildup in the body. Finally, myocardial infarction, commonly called heart attack, happens when a blood clot develops at the site of plaque in a coronary artery and suddenly cuts off most or all blood supply to that part of the heart muscle. Cells in the heart muscle begin to die if they do not receive enough oxygen-rich blood. The result can be permanent damage to the heart muscle or death.
Cardioprotective doses of thyroid hormones improve NO bioavailability in erythrocytes and increase HIF-1α expression in the heart of infarcted rats
Published in Archives of Physiology and Biochemistry, 2022
Alexandre Luz de Castro, Rafael Oliveira Fernandes, Vanessa D. Ortiz, Cristina Campos, Jéssica H. P. Bonetto, Tânia Regina G. Fernandes, Adriana Conzatti, Rafaela Siqueira, Angela Vicente Tavares, Adriane Belló-Klein, Alex Sander da Rosa Araujo
Acute myocardial infarction is an ischaemic pathology of the heart that involves an irreversible loss of cardiomyocytes, leading to a decrease in cardiac function (Schenkel et al. 2010). This condition is a leading cause of morbidity and mortality (Hong et al. 2019). Besides that, myocardial infarction is also associated with a decrease in nitric oxide (NO) bioavailability in the heart and in the red blood cells (Eligini et al. 2013, De Castro et al. 2015). The maintenance of NO levels in the cardiac tissue is important, mainly after the ischaemic injury, since this molecule can upregulate the expression of the hypoxia inducible factor-1α (HIF-1α) by activating the phosphatidylinositol 3-kinase (PI3K)-Akt pathway (Sandau et al. 2000, Kasuno et al. 2004). Activation and upregulation of HIF-1α has been recently found to be a protective mechanism against ischemia-reperfusion injury in the heart (Alchera et al. 2008, Zhong et al. 2008).
Comprehensive viewpoints on heart rate variability at high altitude
Published in Clinical and Experimental Hypertension, 2023
Jun Hou, Keji Lu, Peiwen Chen, Peng Wang, Jing Li, Jiali Yang, Qing Liu, Qiang Xue, Zhaobing Tang, Haifeng Pei
Myocardial infarction is a common clinical cardiovascular disease characterized by the occlusion or rupture of coronary lipid plaques or continuous spasm of the coronary artery, resulting in coronary stenosis or even complete occlusion, leading to myocardial ischemia and injury. In high-altitude environments, the likelihood of inducing coronary artery spasm and myocardial infarction is higher. In addition to specific ST-segment elevation observed on dynamic electrocardiograms, changes in HRV become more pronounced, and the LF/HF ratio decreases (90,91,104,105). High-altitude hypoxia can stimulate the activation of certain inflammatory mediators, such as NLRP3 inflammatory corpuscles, which may contribute to cardiomyopathy (92). The underlying mechanism may be related to mitochondrial autophagy under hypoxia (93). Kujime et al. reported a case of Takotsubo cardiomyopathy syndrome in which HRV’s LF and HF components were significantly suppressed, and these changes were observed earlier than alterations in ECG waveforms. Compared with the ECG during the healing period, the abnormality in HRV on the actual onset day was more pronounced (94). However, this study was a case report, and its accuracy requires further investigation.
Takotsubo cardiomyopathy and its variants: a case series and literature review
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Syed Mustajab Hasan, Jay D. Patel, Mohammed Faluk, Jigar Patel, Premranjan Singh
Patients typically present with symptoms classic of an acute myocardial infarction which include acute and unstable substernal, pressure like chest pain, shortness of breath, palpitations, or arrhythmia. In the more severe cases involving severe left ventricular outflow tract obstruction, patients may also be in cardiogenic shock. Additionally, EKG changes classic of acute ST-segment elevation myocardial infarction are also seen but follow-up catheterization does not reveal coronary artery disease in the location of myocardial dysfunction. Important complications to keep in mind are as follows. Firstly, right ventricular involvement occurs from 18% to 34% of patients and has been associated with other complications such as lower EF, worsening heart failure, pleural effusions, and even longer hospital course. Other factors that were related to heart failure, cardiogenic shock, and longer hospital course were the presence of left ventricular outflow tract obstruction, acute mitral regurgitation, new-onset atrial fibrillation, thrombus formation due to akinetic myocardium, pericardial effusion, or ventricular-free wall rupture [4,9–16].
Related Knowledge Centers
- Angina
- Heartburn
- Infarction
- Lightheadedness
- Shortness of Breath
- Ischemia
- Nausea
- Heart
- Cardiac Muscle
- Coronary Arteries
- Shortness of Breath