Misdiagnosis Of Myocardial Infarction Research Articles

Learning from an analysis of closed malpractice litigation involving myocardial infarction

ObjectiveTo examine the epidemiologic data, identify the pattern of dispute, and determine clinical litigious errors by analyzing closed malpractice claims involving myocardial infarction (MI) in Taiwanese courts. MethodsA retrospective descriptive study was performed to analyze the verdicts pertaining to MI from the population-based database of the Taiwan judicial system between 2002 and 2013. The results of adjudication, involved specialists, primary dispute leading to lawsuits, and litigious errors were recorded. ResultsA total of 36 closed malpractice claims involving MI were included. The mean interval between the incident and litigation closure was 65.5 ± 28.3 months. Nearly 20% of the cases were judged against clinicians and the mean payment was $100639 ± 49617, while the mean imprisonment sentence was 4.3 ± 1.8 months. Cardiologists and emergency physicians were involved in 56.3% of cases, but won 92.6% of lawsuits, while other specialists lost nearly 25% of lawsuits. The most common dispute was misdiagnosis (38.9%), but this dispute had the lowest percentage of loss (7.1%). Disputes regarding delayed diagnosis were judged against the defendants in 50% of claims. Clinicians lost the lawsuit in the following conditions: 1) misdiagnosis of MI in patients with typical chest pain and known coronary artery risk factors; 2) failure to perform thoughtful evaluation and series investigations in patients suspicious of ischemic heart disease; 3) failure to perform indicated treatment to avoid disease progression. ConclusionsMedical practitioners should keep a high index of MI suspicion, especially if the diagnosis and treatment of MI are beyond their daily practice. Prudent patient reevaluation, serial ECG and cardiac enzyme testing, and early consultation are suggested to reduce malpractice liability.

Strategies to overcome misdiagnosis of type 1 myocardial infarction using high sensitive cardiac troponin assays.

High sensitive cardiac troponin assays have become the gold standard in the diagnosis of an acute type 1 myocardial infarction (MI) in the absence of ST-segment elevation. Several acute or chronic conditions that impact cardiac troponin levels in the absence of a MI might lead to a misdiagnosis of MI. For example, patients with impaired renal function as well as elderly patients often present with chronically increased cardiac troponin levels. Therefore, the diagnosis of MI type 1 based on the 99th percentile upper limit of normal threshold is more difficult in these patients. Different diagnostic approaches might help to overcome this limitation of reduced MI specificity of sensitive troponin assays. First, serial troponin measurement helps to differentiate chronic from acute troponin elevations. Second, specific diagnostic cut-offs, optimized for a particular patient group, like elderly patients, are able to regain specificity. Such an individualized use and interpretation of sensitive cardiac troponin measurements improves diagnostic accuracy and reduces the amount of misdiagnosed MI type 1.

Elevation of skeletal muscle isoform of serum creatine kinase in heterozygous familial hypercholesterolaemia

Serum creatine kinase (CK) is an important adjunct in the diagnosis of myocardial infarction or in monitoring for the side-effects of drugs. We report elevation of CK in patients with untreated heterozygous familial hypercholesterolaemia (FH) with no evidence of myocardial infarction. Of a group of 30 patients, 60% had elevated CK values on one occasion. In 40% of patients elevated CK activity was observed on most occasions. This was not related to exercise or previous lipid-lowering therapy. These observations are of importance in view of the potential for misdiagnosis of myocardial infarction or premature withdrawal of lipid-lowering therapy.

Differentiation of creatine kinase MB and IgA-linked BB isoenzymes on electrophoresis

IgA-linked creatine kinase (CK, EC 2.7.3.2) is a macro CK type 1 isoenzyme that has an identical electrophoretic mobility to CK-MB. Its presence has the potential of causing misdiagnosis of myocardial infarction. Mixing anti-CK-B antiserum with the sample prior to electrophoresis did not unequivocally distinguish between the two isoenzymes. Similarly, anti-human IgG and IgM antibodies were also ineffective. However, the IgA-linked isoenzyme band was removed by anti-human IgA antiserum. While anti-CK-M antibodies did not affect the electrophoretic mobility of IgA-linked CK-BB, the antibody eliminated both the CK-MB and CK-MM bands. Thus, specific anti-IgA and anti-CK-M antibodies may be used to establish the presence of the myocardial isoenzyme.