Myocardial infarction characteristics

As research continues and as analytical methodology becomes more precise we find a higher resolution of some lipoprotein classes and better definition of their roles. One example is lipoprotein (a) (lp(a)), first described in 1963. Lipoprotein (a) is an LDL whose normal apoprotein (apo B) is linked to an additional protein, apoprotein a, via a disulfide bridge. Lipoprotein (a) interferes with normal fibrinolysis leading to an increased prevalence of blood clots, and is thought to present an especially high risk for myocardial infarction. Characteristics and functions of lipoproteins are described in Table 3. 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

Ventricular premature depolarizations occur as a result of abnormal ventricular automaticity, as a result of enhanced activity of the sympathetic nervous system and altered electro-physiologic characteristics of the heart during myocardial ischemia and following myocardial infarction. 

It is important to realize, that diseases such as myocardial infarction or type 2 diabetes represent a heterogeneous group of several distinct subphenotypes definable by clinical or biochemical characteristics. Thus, contradictory findings in pharmacogenomic studies may only not be the consequence of a lack of a major isolated gene effect (of the gene variant studied) and chance findings, but also be caused by the variability in the mix of distinct clinical phenotypes hidden beneath a common characterization such as type 2 diabetes and modulated by differences in the environment between studies. 

Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up. Circulation 1978 58 679-88. 

Fig. 5.3 Results of TACTICS TIMI 18. Primary end point of death, non-fatal myocardial infarction, and rehospitalization for acute coronary syndrome at 6 months based on baseline patient characteristics ( 2001 Massachusetts Medical Society)...

E Role in therapy Thrombolytic agents currently licensed for the treatment of AMI in the United States include streptokinase, tissue plasminogen activator, anistreplase, reteplase, and tenecteplase. TNKase and alteplase have similar clinical efficacy for thrombolysis after myocardial infarction (i.e., similar mortality and intracranial hemorrhage rates). However, advantages of TNKase include ease and rapidity of administration, longer half-life, greater fibrin specificity, and lower noncerebral bleeding rates. Reteplase shares some characteristics of tenecteplase (e.g., similar half-life, rapid onset, and ease of administration). 

One of the most important chronic alterations in the heart is the chronic phase after myocardial infarction. The postinfarction period is known to be associated with an increased risk for sudden cardiac death and for the occurrence of cardiac arrhythmia. Changes in conduction properties have been identified [Dillon et al., 1988], although the cells exhibit normal or near normal action potential characteristics [Wit and Janse, 1992]. Thus, cellular electrophysiology does not explain the complete pathophysiology of the arrhythmogenic substrate. Thus, other factors, for example structural changes and passive electrical properties, have to be taken into account. 

O Mental retardation, osteoporosis, myocardial infarction, and a characteristic dislocation of the lens occur. 

Antman developed a thrombosis in myocardial infarction (TIMI) risk score based on a database of 15,078 patients with STEMI or new onset of complete left bundle branch block (8), The score was validated in the TIMI 9 data set. Ten characteristics of these patients accounted for 97% of the predictive capacity of their multivariate model. These are included in the risk score (Table I). Points were given for difference parameters as listed in Table I. The risk score had a strong association with 30-day mortality. There was a greater >40-fold increase in mortality from TIMI risk score 0 to >8 at 30 days (Table I) (8), The TIMI risk score is easy to apply and can be done at the bedside. 

An example of an enzyme which has different isoenzyme forms is lactate dehydrogenase (LDH) which catalyzes the reversible conversion of pyruvate into lactate in the presence of the coenzyme NADH (see above). LDH is a tetramer of two different types of subunits, called H and M, which have small differences in amino acid sequence. The two subunits can combine randomly with each other, forming five isoenzymes that have the compositions H4, H3M, H2M2, HM3 and M4. The five isoenzymes can be resolved electrophoretically (see Topic B8). M subunits predominate in skeletal muscle and liver, whereas H subunits predominate in the heart. H4 and H3M isoenzymes are found predominantly in the heart and red blood cells H2M2 is found predominantly in the brain and kidney while HM3 and M4 are found predominantly in the liver and skeletal muscle. Thus, the isoenzyme pattern is characteristic of a particular tissue, a factor which is of immense diagnostic importance in medicine. Myocardial infarction, infectious hepatitis and muscle diseases involve cell death of the affected tissue, with release of the cell contents into the blood. As LDH is a soluble, cytosolic protein it is readily released in these conditions. Under normal circumstances there is little LDH in the blood. Therefore the pattern of LDH isoenzymes in the blood is indicative of the tissue that released the isoenzymes and so can be used to diagnose a condition, such as a myocardial infarction, and to monitor the progress of treatment. 

Patients who are heterozygotes for familial hypercholesterolemia (FH) have plasma LDL levels that are two- to threefold that of the normal population, so that they are in the upper fifth percentile of LDL cholesterol for their age. About 50% of men and 15% of women with this trait have at least one myocardial infarct by the age of 60. Approximately 1 in 500 persons has inherited this abnormality, which is inherited as an autosomal dominant characteristic (G20). 

Danish Investigations of Arrhythmia and Mortality ON Dofetilide. Dofetilide in patients with left ventricular dysfunction and either heart failure or acute myocardial infarction rationale, design, and patient characteristics of the DIAMOND studies. Clin Cardiol 1997 20(8) 704-10. 

Generally, the clinical presentation of myocardial ischaemia is the characteristic pain known as angina pectoris or some equivalents (e.g. dyspnoea), although sometimes ischaemia may be silent (see Silent ischaemia , p. 302). If the anginal pain is new or if it has increased with respect to previous discomfort (crescendo angina), this constitutes the clinical condition called acute coronary syndrome (ACS), which may evolve into myocardial infarction (MI) (see Section Acute coronary syndrome , p. 209). If the angina pain appears with exercise... 

Lamfers EJ, Hooghoudt TE, Herzberger DP, Schut A, Stol-wijk PW, Verheugt FW. Abortion of acute ST segment elevation myocardial infarction after reperfusion incidence, 6 kifeiie characteristics and prognosis. Heart 2003 89 496. 

Sadanandan S, Hochman S, Kolodzjez A et al. Clinical and electrocardiographic characteristics of patients with combined anterior and inferior ST segment elevation in the initial ECG during acute myocardial infarction. Am Heart J 2003 146 653. 

Interruption of the heart s blood supply leads to the death of cardiac muscle cells. The symptoms of myocardial infarction include pain in the left side of the chest that may radiate to the neck, left shoulder, and arm, and irregular breathing. The initial diagnosis is based on these and other symptoms. Therapy is instituted immediately. Physicians then use several enzyme assays to confirm the diagnosis and to monitor the course of treatment. The enzymes most commonly assayed are creatine kinase (CK) and lactate dehydrogenase (LDH). Each enzyme s activity shows a characteristic time profile in terms of its release from damaged cardiac muscle cells and rate of clearance from blood (Figure 6A). 

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