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==Malaria Induced Myocardial Infarction==

Epidemiology
With 225 million people affected by malaria worldwide and 2.3 million annual deaths per year due to cardiovascular disease, many people are at risk for malaria induced myocardial infarction. Nonetheless, myocardial involvement in malarial infection has not been studied extensively. Only recently have studies on volume resuscitation and pulmonary edema in severe cases of malaria suggested that there is a link between malarial infection and myocardial infarction. One such study followed a cohort of hospital patients infected with the disease and observed a statistically significant increase in risk of heart attack, from 0.82% for those without malaria to 1.43% in those infected with the disease.

Genetic Component
There have also been findings linking the two diseases genetically. In April 2011, scientists discovered that regulation of plasma Inter-Cellular Adhesion Molecule 1 (ICAM-1) levels are carried out by six specific genetic loci, which include ABO, ICAM1, NFKBIK, PNPLA3, RELA and SH2B3. Soluble ICAM-1 or sICAM-1 is an inflammatory marker expressed on the surface of endothelial and immune system cells. ICAM-1 is associated with many conditions, including malaria and a risk factor for myocardial infarction. Scientists hypothesize that the body’s pro-inflammatory response following malarial infection plays a role in the body’s increased risk for heart attack. After the plasmodium enters the blood supply, it releases tyrosyl-tRNA synthetase (PfTyrRS), a housekeeping protein translation enzyme, which then infects red blood cells and is internalized by host macrophages. This PfTyrRS-macrophage complex triggers the release of pro-inflammatory cytokines and causes the up-regulation of endothelial ICAM-1 receptors, which, in turn, increase the risk of myocardial infarction. Because PfTyrRS begins the pro-inflammatory response pathway that increases the risk of heart attack, it provides a new target for anti-infarctic and malarial drugs.

Pathophysiology
Although the exact pathophysiology underlying malarial induced heart attack remains unclear, scientists have several hypotheses as to how malarial infection causes myocardial injury. One study noted that that patients with the infection showed acidosis and hypoglycemia, primarily due to hypovolemia, which led to myocardial impairment and damage. Cardiac damage was measured by an increase in the level of circulating cardiac proteins, N-terminal pro-brain natriuretic peptide (NT-proBNP) and heart-type fatty acid-binding protein (H-FABP). NT-proBNP is a neurohormone secreted in response to high wall tension and an indicator for reduced functions of the left ventricle, while H-FABP is an intracellular molecule that assists in the conveyance of fatty acids in myocardial cytoplasm. Moreover, both biomarkers are strong indicators of myocardial infarction. Another hypothesis is that factors such as ischaemia, acidosis, toxic effects of substances like P. falciparum glycosyl-phosphatidyl-inositol, or Plasmodium triggered mechanisms like apoptosis can cause damage to the heart. Lastly, elevated levels of catecholamine have been associated with damage to the heart by causing vasoconstriction. Welcome. We use review articles per WP:MEDRS. Thanks. Doc James (talk · contribs · email) 11:53, 23 December 2011 (UTC)