Left Ventricular Rupture in Transmural Myocardial Infarction Without Enzymatic or Electric Disturbances: Medico-legal Implications

Mesrati MA1*, Boussaid M1, Mahjoub Y1, Sahnoun M1, Boughattas M1, Chadly A2 and Aissaoui A1 1Department of Forensic Medicine, TaherSfar Hospital, Mahdia, Tunisia 2Department of Forensic Medicine, Fattouma bourguiba Hospital, Monastir, Tunisia *Corresponding author: Mesrati Mohamed amine, Department of Forensic Medicine, TaherSfar Hospital, Mahdia, Tunisia; Tel: 21650554425; Email: mesrati.amin@gmail.com


Introduction
Left ventricular free wall rupture (LVFWR) is a rare and fatal complication of acute myocardial infarction (AMI). The early and accurate identification of myocardial necrosis in patients experiencing features suggestive of acute coronary syndrome is an important challenge. It depends upon the interpretation of the patient's history, electrocardiographic and cardiac markers data [1]. However, these parameters are known to be unspecific and sometimes non-diagnostic or unequivocal [2]. Thus, the diagnosis of myocardial infarction may be misleadingly unnoticed which may harm patients and result in increased morbidity or death. In this case, Doctor's liability may be engaged for missed diagnosis.
We aim to report an autopsy case of transmural myocardial infarction complicated with Left ventricular free wall rupture in a patient without enzymatic or electric disturbances and we discuss the physician's responsibility.

Case Presentation
A 48-year-old man, without past medical history, was admitted into the Emergency Department of a Peripheral Health Center because of chest tightness of two days duration.
Physical examination did not reveal any abnormalities, despite an elevated blood pressure (170/110 mmHg). Per critical electrocardiogram was unremarkable ( Figure 1). Specially, it did not reveal ST segment and T wave abnormalities. No electrocardiographic changes evolved 2 hours later ( Figure 2). Results of laboratory tests were within normal limits: enzymatic cardiac levels (total Creatine Phosphokinase) were at 140 UI (normal 0-185 U/L), CK-MB to CK ratio was <5%, and the dosage of troponin I was technically impossible (lack of reagent). Transthoracic echocardiogram did not highlight cardiac failure or kinetic trouble (left ventricular function at 63%). The pericardial sac was free of effusion. Thus, the patient was discharged with the diagnosis of parietal pain. He was confined to bed during his stay at home because of persisting chest pain. Two days later, he presented syncope and arrived dead to hospital.

Discussion
The diagnosis of AMI can be a challenging task for many physicians in an emergency department. It was previously based on the criteria set by the World Health Organization (WHO). A patient is diagnosed with myocardial infarction if he presents two of the following 1: typical history of ischaemic type chest pain; 2: changes on serial ECG tracing; 3: typical rise and fall of serum cardiac enzymes [3]. However, each of these variables is known to lack precision.
In fact, a history of prolonged chest pain is often absent in patients with infarction, and when present, it may be due to other events than myocardial ischemia [4]. The ECG is also an important tool for detecting AMI. When typical changes of AMI are present on the admission ECG (ST elevation and new Q-wave), they are quite specific and have a very high positive predictive value for the diagnosis, but their absence should not rules it out, as many as 30-50% of patients may initially present with normal or non-diagnostic ECG [5]. Johnson WJ [5] reported that new Q wave changes on electrocardiograms in patients with myocardial infarction are absent in approximately 30% of autopsy-proven cases. Wagner et al. [2] identified 29 of 84 patients with definite infarction but falsely negative ECG.
Because of the above, the WHO criteria were refined to give more prominence to cardiac biomarkers [3]. The joint European Society of Cardiology/ American College of Cardiology Committee, redefines myocardial infarction according to cardiac markers as an increase in cardiac troponin cTnI, cTnT or an increase in creatine Kinase muscle and brain (CK-MB) [6]. Nowadays, most physicians rely heavily on serum level changes of cardiac enzymes to retain or exclude the diagnosis of acute myocardial infarction. Cardiac markers play an important role in this field when the patient's history and ECG are non-diagnostic or misleading [7]. Creatine kinase (CK) is one of the oldest biochemical markers of myocardial damage. It has a clinical sensitivity of 90% for the diagnosis of AMI. Unfortunately, this is not matched by high specificity. It is released within 12 hours after symptom onset of AMI, peaks in serum at 24-36 hours, and returns to normal in 48-72 hours. As a result of these release kinetics, measurement of total CK is not suitable for the early diagnosis (within 6 hours) of AMI [8] and serial sampling is the most effective method for that aim [9]. In this case report, the exclusion of the diagnosis of AMI was based only on one single value of CK at presentation which appears to be unreliable. CK as a marker is also unsuitable for the detection of myocardial damage that may occur in patients presenting with Non-ST elevation myocardial infarction like in this case report.
A marker that is suitable for the early diagnosis of AMI and the detection of small injuries to the heart should be abundant in the myocardium and not present in other tissues, have a total cardiac specificity with undetectable plasma concentration and finally it should be released completely and quickly when myocardial damage occurs [10]. CK does not fulfill these criteria since it is widely distributed in the body and have a high range up to 200 IU/L [9]. In the other hand, there are cases of AMI without elevation of total CK concentration. This situation leads to the failure to accurately diagnose the myocardial ischaemic damage and delays in the initiation of appropriate treatments [11]. As a result and to improve on the cardiac specificity of CK for the diagnosis of AMI, it was recommended to measure both total CK and CK-MB (the cardiac specific isoenzyme of CK). A CK-MB to CK ratio up to 6% is reported to be specific for myocardial injury [10]. In this case report, the ratio was <5%. This is may be explained by the delay from the onset of the symptoms which is >48 h. Thus, the diagnosis value of CK-MB will be applicable only to patients who are seen early after the onset of symptoms. Wagner et al [2] reported that the absence of CK-MB in patients who are seen more than 24h remote from the onset of their acute episode may not be used as evidence for exclusion of the diagnosis AMI. However, physicians should keep in mind that there are various non-cardiac causes for elevated CK-MB like severe skeletal muscle damage. In these situations, cardiac troponins can be used to differentiate cardiac and non-cardiac pathologies. Elevated troponins concentrations have been reported to be a specific marker for the diagnosis of AMI. Their clinical sensitivity approaches 100% at about 12h after symptom onset [12].
Myocardial rupture is a catastrophic complication of AMI that directly causes death in 8% of cases [13]. It occurs within 7 days, in 1-4% of patients with AMI [14]. It may occur in patients with their first transmural AMI like in our case. Prodromal manifestations reported in the literature are intractable vomiting, restlessness, persistent chest pain, cardiovascular collapse… In the case reported here, death occurred 2 days after the onset of the symptoms, which suggest a subacute or stuttering ruptures. This implies a gradual or incomplete ruptures of the infarcted area with slow bleeding in the pericardial sac causing progressive cardiac tamponade [14].
The above reported case showed how much paraclinical features of AMI can be misleading. Previous studies have shown that between 4% and 8% of patients with missed AMI are sent home [15]. This finding confirms the relatively low rate of missed AMI patients reported by Lee et al (3.8% of missed diagnosis) [16] and McCarthy et al (2%) [17]. diagnosed cases can lead health professionals to legal suits. Accordingly, misdiagnosis of AMI is a common cause for malpractice claims. In the United States, diagnostic errors become the most prevalent type of malpractice claim [18]. Unrecognized AMI frequently involved multiple breakdowns. The leading contributing factors related to the misdiagnosis of acute chest pain in the emergency department are failure to perform an adequate history or physical examination, failure to identify atypical presentation, failure to order or misinterpret an appropriate diagnostic test and failure to order an appropriate specialized consultation [19]. The claims about diagnostic error can be usually subject to trials in both of penal judgment and compensation trial. According to the Tunisian Criminal Code (TCC), doctors can be prosecuted under section 225(involuntary assault by negligence or inattention) which is punishable with imprisonment for a term that may extend to 1 year. They are also being punished for involuntary homicide, if death occurs, under section 217 of the TCC. Also, the doctor can be made liable in civil law for paying compensation and damages.
Thus, for quality assurance and to avoid the failure to recognise AMI, physicians should be more aware and consider atypical presentations, document more detailed histories, do not accurately rely on paraclinical tests (ECG and cardiac markers) and readily admit patients with vague or suspicious symptoms. McCarthy et al. [17] have reported that 25% of missed AMIs might have been prevented by not sending home patients with symptoms believed to be due to ischemic heart disease. This reinforces the idea that unequivocal symptoms should provoke discussion among emergency physicians to avoid erroneous discharge.