241 The role of ischemic mitral regurgitation in the development of heart failure following acute myocardial infarction

Among possible pathogenic and adaptive mechanism of acute myocardial infarction and development of its complications, the system of prostanoids, particularly prostacycline-thromboxane system is of prime importance. But many questions relating the role of prostacycline-thromboxane system in pathogenesis of myocardial infarction associated with heart failure have studied insufficiently. The objective of this work is to study the ststus of prostacycline-thromboxane system in patients of acute myocardial infarction associated with heart failure and its correlation with the platelet functions depending on stages of heart failure. This study was performed in the department of Internal Medicine in Kharkov State Medical Institute, Ukraine in 1985-89. 120 patients with acute myocardial infarction leading to heart failure were studied. The status of prostacycline-thromboxane was considered by the level of stable metabolites of prostacycline and thromboxane - A2 as 6-keto-PGF and TXB2 respectively in venous plasma. 6-Keto-PGF-1a and TXB2 levels were determined by Radio-immunological method with the help of kits manufactured by the English Firm "New England Nuclear". To determine the platelet aggregation properties, the instrument "Bian-120" transmitter was used. It was established clinically that prostacycline- thromboxane activation depends on clinical features of myocardial infarction, i.e. its localization, depth, extension or affected size of MI, first attack or re-infarction. Maximum changes of prostacycline thromboxane system took place in extensive myocardial infarction which was expressed in increased level of TXB2 and significant change of prostanoid imbalance ratio. Parameters of platelet aggregation function and prostacycline thromboxane system were interrelated during heart failure, which were expressed by their changes in aggregation diagram.Medicine Today 2014 Vol.26(2): 83-87

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Using human genetics to understand the causes and consequences of circulating cardiac troponin I in the general population

10.1101/2020.09.04.20187401 ◽

2020 ◽

Author(s):

Marta R Moksnes ◽

Helge Røsjø ◽

Anne Richmond ◽

Magnus N Lyngbakken ◽

Sarah E Graham ◽

...

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Acute Myocardial Infarction ◽

General Population ◽

Cardiac Troponin ◽

Troponin I ◽

Mendelian Randomization ◽

Cardiac Troponin I ◽

Health Study

AbstractCirculating cardiac troponin proteins are associated with structural heart disease and predict incident cardiovascular disease in the general population. However, the genetic contribution to cardiac troponin I (cTnI) concentrations and its causal effect on cardiovascular phenotypes is unclear. We combine data from two large population-based studies, the Trøndelag Health Study and the Generation Scotland Scottish Family Health Study and perform a genome-wide association study of high-sensitivity cTnI concentrations with 48 115 individuals. We further used two-sample Mendelian randomization to investigate the causal effects of circulating cTnI on acute myocardial infarction and heart failure.We identified 12 genetic loci (8 novel) associated with cTnI concentrations. Associated protein-altering variants highlighted putative functional genes: CAND2, HABP2, ANO5, APOH, FHOD3, TNFAIP2, KLKB1 and LMAN1. Phenome-wide association tests in 1283 phecodes and 274 continuous traits in UK Biobank showed associations between a polygenic risk score for cTnI and cardiac arrhythmias, aspartate aminotransferase 1 and anthropometric measures. Excluding individuals with a known history of comorbidities did not materially change associations with cTnI. Using two-sample Mendelian randomization we confirmed the non-causal role of cTnI in acute myocardial infarction (5 948 cases, 355 246 controls). We found some indications for a causal role of cTnI in heart failure (47 309 cases and 930 014 controls), but this was not supported by secondary analyses using left ventricular mass as outcome (18 257 individuals).Our findings clarify the biology underlying the heritable contribution to circulating cTnI and support cTnI as a non-causal biomarker for acute myocardial infarction and heart failure development in the general population. Using genetically informed methods for causal inference of cTnI helps inform the role and value of measuring cTnI in the general population.

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