Pseudoaneurysm originating from left ventricle aneurysm: An autopsy case and review of literature

Rupture of the free wall of the left ventricle is a catastrophic complication of acute myocardial infarction. Rarely, free wall rupture is contained by overlying adherent pericardium, producing a pseudoaneurysm of the left ventricle. In this report, a case of a left ventricular pseudoaneurysm due to a previous myocardial infarction is described. A 55-year-old woman had a severe chest pain 11 months prior to death. No cardiac investigation was performed. Three days prior to death, she suffered from fatigue and weakness, and had a witnessed sudden cardiac death. At autopsy, a 8.5 × 10 × 8 cm pseudoaneurysm of the left ventricle was found. There was severe coronary artery atherosclerosis. There were extensive adhesions between pericardium and pseudoaneurysm wall. The cause of death was attributed to heart failure and resulting arrhythmia. The case illustrates the rare event of left ventricular pseudoaneurysm first diagnosed at forensic autopsy.     

Sudden perinatal death due to rupture of congenital cardiac diverticulum. Pathological findings and medico-legal investigations in malpractice charge

Congenital diverticula of the left ventricle, very rare malformations, are determined by an abnormal embryonic development of the ventricular wall and can be isolated or associated to other cardiac anomalies. In most of the cases, these pathologies are not symptomatic and in some patients can be associated to ventricular arrhythmia, cardiac rupture with tamponade and sudden death.Authors are presenting the case of a sudden death in an 8-weeks-old newborn due to rupture of a cardiac congenital diverticulum of the left ventricle, discovered only at the moment of the autopsic examination. The parents of the victim pressed charges against the medical staff that was appointed to the cares, blaming them with malpractice.The missed diagnosis of a cardiac congenital diverticulum of the left ventricle, a rare pathology, reflects the trickiness of the medical management that can lead to medico-legal controversies and, even though such rare conditions must be always taken into consideration when investigating possible dysfunction causing the death, diagnostic difficulties, in the case in exam, justify the missed diagnosis intra-vitam of cardiac ventricular diverticulum.     

An autopsy case of cardiac tamponade caused by a ruptured ventricular aneurysm associated with acute myocarditis

We report an autopsy case of hemopericardium caused by rupture of a ventricular aneurysm associated with acute myocarditis in an infant boy aged 2 years and 10 months. Three days before his death, the patient developed fever. On the day of death, he described an urge to defecate and attempted to do so in an upright position. While straining to defecate without success for a prolonged period, he stopped breathing and collapsed. On autopsy, his heart weighed 91.7 g and cardiac tamponade was evident, the pericardial cavity being filled with 140 mL of blood that had come from a 1.5-cm-long rupture in a 2.7 × 1.5 cm ventricular aneurysm in the posterior left ventricular wall. Patchy grayish-white discoloration was noted in the myocardium. Histologically, CD3-positive T lymphocytic infiltration accompanied by pronounced macrophage infiltration was observed in the myocardium. Hemorrhagic necrosis was detected in the area of the ventricular aneurysm. Staining for matrix metalloproteinase (MMP) expression revealed abundant MMP-2, MMP-7, and MMP-9. Polymerase chain reaction to detect viruses failed to identify any specific causative viruses in the myocardium. In this case of lymphocytic (viral) and histiocytic myocarditis with pronounced macrophage infiltration and upregulation of MMP expression, myocardial remodeling and associated wall weakening had resulted in formation and rupture of an aneurysm.     

Indium-111-antimyosin images compared with triphenyl tetrazolium chloride staining in a patient six days after myocardial infarction.

The results of indium-111 (111In) antimyosin imaging during life and the findings on postmortem imaging and triphenyl tetrazolium chloride (TTC) staining of the heart are reported from a patient who received 111In-antimyosin on the sixth day following myocardial infarction and died after imaging the next day. The planar images obtained during life showed abnormal 111In-antimyosin uptake in the posterior, lateral, and apical walls of the left ventricle. Autopsy revealed extensive infarction of the left ventricular lateral and posterior walls with cardiac rupture, which was the cause of sudden death. Direct imaging of the sliced specimen of heart revealed abnormal tracer uptake in the lateral and posterior walls of the left ventricle, which correlated closely with the area of necrosis outlined by TTC staining. Our results confirm the experimental findings that antimyosin antibody binds specifically to the acute irreversibly damaged myocardial cells. A high degree of tracer uptake can be seen even when 111In-antimyosin is injected six days postinfarction.     

Feasibility of post mortem cardiac proton density weighted fast field echo imaging in two cases of sudden death

ObjectiveThe aim of this work is to investigate and compare cardiac proton density (PD) weighted fast field echo (FFE) post-mortem magnetic resonance (PMMR) imaging with standard cardiac PMMR imaging (T₁-weighted and T₂-weighted turbo spin-echo (TSE)), postmortem CT (PMCT) as well as autopsy.Materials and methodsTwo human cadavers sequentially underwent cardiac PMCT and PMMR imaging (PD-weighted FFE, T₁-weighted and T₂-weighted TSE) and autopsy. The cardiac PMMR images were compared to each other as well as to PMCT and autopsy findings.ResultsFor the first case, cardiac PMMR exhibited a focal region of low signal in PD-weighted FFE and T₂-weighted TSE images, surrounded by a signal intense rim in the T₂-weighted images. T₁-weighted TSE and PMCT did not appear to identify any focal abnormality. Macroscopic inspection identified a blood clot; histology confirmed this to be a thrombus with an adhering myocardial infarction.In the second case, a myocardial rupture with heart tamponade was identified in all PMMR images, located at the anterior wall of the left ventricle; PMCT excluded additional ruptures. In PD-weighted FFE and T₂-weighted TSE images, it occurred hypo-intense, while resulting in small clustered hyper-intense spots in T₁-weighted TSE. Autopsy confirmed the PMMR and PMCT findings.ConclusionsPresented initial results have shown PD-weighted FFE to be a valuable imaging sequence in addition to traditional T₂-weighted TSE imaging for blood clots and myocardial haemorrhage with clearer contrast between affected and healthy myocardium.     

Acute myocardial infarction in a young woman: Unexpected findings of a coronary occlusion

In clinical and forensic practice, the cause of death is often attributed to acute myocardial infarction, among which the coronary atherosclerosis being the Captain of the Men of Death. However, other reasons such as coronary septic embolization with neutrophilic granulocyte myocarditis although rare, can also cause sudden unexpected death. This paper reports a case with this rare cause—a 21-year-old woman diagnosed with “acute gastroenteritis” who died 4 days later. A forensic autopsy revealed an inflammatory polypous embolic located at 1.0 cm from the left anterior descending branch (LAD) with serve neutrophilic granulocyte myocarditis, which resulted in embolic at the opening of the left main coronary artery, acute myocardial infarction and eventually leading to her death. Histopathological examination showed large amounts of neutrophilic granulocyte infiltration in the arterial layer forming the septic embolic and eventually resulting in coronary occlusion. To find the real cause of septic embolic, myocarditis, bacterial, fungal, protozoan and virus detection was performed through RT-PCR, with negative findings. Septic embolic leading coronary occlusion in left main coronary artery and LAD is rarely reported in forensic practice, we hope this report can pave the way on understanding this rare disease to make correct diagnosis in medical practice.     

Right ventricular mural thrombus caused by myocardial infarction diagnosed by computed tomography

Thrombi of the left ventricle are common sequelae to acute anterior myocardial infarctions that involve the apex of the heart and produce akinetic or dyskinetic wall thickening patterns. While infarctions of the right ventricle are being increasingly recognized in the setting of inferior myocardial infarcts, little data on in vivo clot formation in the right ventricle of the heart are available in these patients. In the current study we were able to demonstrate a right ventricular mural thrombus using gated computed tomography of the heart. Although an abnormality in the right ventricle extending from the septal margin of the ventricle into the outflow tract could be identified with standard blood pool computed tomographic images and from cross sectional echocardiograms, only with cardiac gating could the relationship between the mass (thrombus) and the noncontractile section of the right ventricular myocardium be clearly identified. We conclude that cardiac gating may help in the evaluation of cardiac masses, and in particular cardiac thrombi. This will be particular valuable in the setting of recent or remote infarction, as the relationship between wall-motion abnormalities and thrombus formation has been well documented.     

Cardiopulmonary resuscitation does not cause left ventricular rupture of the heart with acute myocardial infarction: a pathological analysis of 77 autopsy cases

Cardiac rupture during acute myocardial infarction (AMI) is one of the most frequent causes of sudden cardiac death. However, some reports have indicated the possibility that the cardiac rupture during AMI may occur by external cardiac massage. We pathologically examined the hearts of 77 patients who died suddenly due to ventricular free wall rupture during AMI (51 men and 26 women; aged 47-94 years; mean age: 69.9 years). We divided the cases into two groups, 44 cases with and 33 cases without cardiopulmonary resuscitation (CPR), and compared the two groups with respect to 12 pathological items. There were no statistical differences in any of the investigated items between the two groups (P>0.05). In addition, mural thrombi were identified along the rupture tract in all cases. Moreover, they were more matured at the subendocardial zone than at the subepicardial or middle zone, irrespective of the groups. From the pathological findings, we concluded that the rupture of the left ventricle during AMI originates from the subendocardial region and precedes the external cardiac massage. Our present study strongly suggests that CPR does not cause the left ventricular rupture of the heart during AMI.     

Morphological identification of right ventricular failure in cases of fatal pulmonary thromboembolism

Pulmonary thromboembolism is a life-threatening event potentially determining right ventricular failure. Even if the pathophysiology of this phenomenon has been widely investigated, no morphological demonstration of right ventricular ischemic damage determining right ventricular failure in cases of fatal pulmonary embolism has been reported till now. We performed an immunohistochemical investigation with the markers fibronectin and C5b-9 in 26 cases of fatal pulmonary thromboembolism (16 ♀, 10 ♂, mean age 56.4 years), as well as in 25 cases of myocardial infarction (16♀, 9♂, mean age 60.8 years) and 20 cases of hanging (3♀, 17♂, mean age 40.8 years). In each case, at least one tissue slide from both cardiac ventricles (free wall of the right ventricle, anterior and/or posterior wall of the left ventricle) was prepared. The reactions were semiquantitatively classified and the groups compared. In the study group, the occurrence of ischemic changes at the right ventricle was significantly higher than in cases of myocardial infarction and global hypoxia due to hanging. The determining aspect of the immunohistochemical examination is the identification of the prevalent ischemic lesion at the right ventricle compared to the left one. This may indicate the primary involvement of the right ventricle thus demonstrating a right ventricular failure.     

Cardiac tamponade secondary to fulminant myocarditis - A case of custodial death

Cardiac tamponade following rupture of the heart occurs very rapidly, resulting in a fatal fall in the cardiac output and circulatory collapse. Spontaneous cardiac rupture is an uncommon occurrence and that too occurring secondary to myocarditis is a very rare event. Myocarditis is an inflammatory disease of the myocardium and its clinical presentation is highly variable. Due to its highly variable clinical presentation, the diagnosis is frequently made at autopsy. In this article, we report death of a prisoner due to cardiac tamponade following right ventricular rupture secondary to fulminant myocarditis.     

A case of a giant left ventricular pseudoaneurysm

A Left ventricular pseudoaneurysm is an outpouching resulting from myocardial free wall rupture which is contained by an adherent pericardium or scar tissue. It most often occurs after transmural myocardial infarction, but may also follow cardiac operations, trauma, inflammation, or infection. In contrast to patients with true ventricular aneurysms, those with false aneurysms most commonly die of hemorrhage.Transthoracic echocardiogram, computed tomography scan and cardiac MRI are currently the noninvasive modalities, whereas coronary arteriography and left ventriculography are invasive modalities used for diagnosis. As this condition is lethal, prompt diagnosis and timely management are vital.We present a case report of a patient with no prior risk factors who presented for 1 year with palpitations during exercise and rest, as well as intermittent chest pain. A transthoracic echocardiogram was performed. Echocardiogram revealed an unexpected outpouching of the left ventricle. A computed tomography scan confirmed the diagnosis by revealing a massive left ventricule pseudomanoeuvre. The patient was offered surgery, but he refused the procedure due to the surgical risk.     

Patent foramen ovale,paradoxical embolism and fatal coronary obstruction

A 75-year-old woman was admitted to the emergency room with chest pain and vomiting. An electrocardiogram and laboratory results were suggestive for myocardial infarction of the posterior cardiac wall. Echocardiography was indicative of aortic dissection, and a CT scan of the thoracic arteries showed a massive pulmonary thromboembolism and thrombotic occlusion of the right coronary artery (RCA). The woman died shortly after admission. Autopsy confirmed the presence of thromboemboli in the right pulmonary artery and its lobar branches. Also, the anterior aortic sinus was filled with a 9 cm long thromboembolus that extended into the RCA, making it dilated and completely occluded. Another 3.5 cm long thromboembolus extended from the beginning of the left subclavian artery. A patent foramen ovale (PFO) was present. On the posterior wall of the left ventricle, there was an area suggestive of myocardial infarction, and histopathological examination confirmed that it was 24–48 hours old. The coronary circulation was “co-dominant”. The sources of thrombotic masses were the deep veins of the lower limbs. The cause of death was myocardial infarction, caused by RCA occlusion with thromboembolus originating from the deep veins of the left lower leg after paradoxical embolism via PFO. This case illustrates that although deep venous thrombosis, pulmonary thromboembolism, and PFO are not rare findings at autopsy, their combination could be a relatively rare cause of fatal coronary artery occlusion after paradoxical embolism.     

A fatal case of intoxication from a single use of eutylone: Clinical symptoms and quantitative analysis results

Eutylone is a synthetic cathinone that is becoming an increasingly popular drug in the US and Europe. This report describes a fatal case of eutylone intoxication. A 32-year-old man went into cardiac arrest after several minutes of abnormal behavior. Rectal temperature was 37.0 °C at 5 h after death. Autopsy revealed no remarkable injuries apart from several small abrasions and no signs of rhabdomyolysis. Toxicological examination revealed only aripiprazole in the therapeutic range and eutylone. The eutylone concentration in cardiac blood was 4290 ng/g. This case is valuable because it involved fatal intoxication from a single use of eutylone and quantitative analysis, whereas most previous reports of eutylone intoxication have involved a mixture of drugs with limited quantitative analysis.     

A forensic autopsy case: Sudden unexpected death due to cardiac inflammatory myofibroblastic tumor

We report an autopsy case of a 25-year-old man with no medical history who died suddenly in an Internet cafe. He was found in cardiorespiratory arrest and did not respond to cardiopulmonary resuscitation. Traumatic lesions were not observed on his body. An autopsy was performed to investigate the cause of death. Upon examination, we discovered a heart tumor that infiltrated from the outside wall to the outflow tract of the left ventricle. Left ventricular outflow tract obstruction due to a cardiac tumor was considered the mechanism of death. Histological examination identified an inflammatory myofibroblastic tumor (IMT). The final diagnosis was death secondary to circulatory failure due to a cardiac IMT. Additionally, a cardiac tumor was diagnosed using post-mortem computed tomography. Only few cases of sudden unexpected death due to cardiac IMT have been reported; we report this case along with a review of the literature.     

Imaging of cocaine-induced global and regional myocardial ischemia

Severe and often fatal cardiac complications have been reported in cocaine users with narrowed coronary arteries caused by atherosclerosis as well as in young adults with normal coronaries. We have found that in normal dogs cocaine induces severe temporary hypoperfusion of the left ventricle as indicated by a significantly lower 201Tl concentration compared to the baseline state. The most significant decrease in uptake occurred 5 min after injection and was more pronounced in the septal and apical segments. Following intravenous administration of cocaine, instead of gradual disappearance of 201Tl from the left ventricle, there was continuous increase in 201Tl concentration in the left ventricle. These imaging experiments indicate that the deleterious effects of cocaine on the heart are probably due to spasm of the coronaries and decreased myocardial perfusion. Since spasm of the large subpericardial vessels does not seem to explain the magnitude of the increased coronary resistance and decreased coronary flow after cocaine as described in the literature, it is suggested that microvascular spasm of smaller vessels plays a major role in the temporary decrease in perfusion. The data may also suggest that severe temporary myocardial ischemia is probably the initiating factor for the cardiac complications induced by cocaine.     

A case of acute myocardial infarction after intracoronary stent implantation: Demonstration of the stent location by postmortem X-ray examination

A 70-year-old man died 1 h after his car was involved in a minor collision with a stationary bus. One month before the accident, he had been diagnosed as having ischemic heart disease due to severe stenosis of the left anterior descending coronary artery (LADCA) by coronary angiography, followed by intracoronary stent implantation. Postmortem examination failed to show any potentially fatal injury, but macroscopic examination demonstrated myocardial necrosis accompanied by massive bleeding in the anterior left ventricle. Since it was difficult to delineate the precise site of the implanted stent in the heart by naked-eye examination, X-ray examination was performed. Guided by X-ray imaging, the stent, measuring 10 mm in length and 2 mm in diameter, was confirmed in the LADCA. Microscopic examination demonstrated myocardial necrosis accompanied by hemorrhage and granulation tissue in the anterior wall of the left ventricle, in the territory of the LADCA downstream from the implanted stent. However, there was no evidence of stent thrombosis. Therefore, it was likely that occlusion had occurred in a branch or branches of the LADCA downstream from the location of the stent. In conclusion, X-ray examination seems to be an effective adjunct in forensic pathology for localization of an implanted coronary stent and careful investigation of the coronary artery surrounding the stent.     

Autopsy case of Rosai–Dorfman disease presenting as fibrinous pericarditis

Rosai–Dorfman disease (RDD) is a rare non-Langerhans cell histiocytosis that is characterized histopathologically by accumulation of CD68-positive, S100-positive, and CD1a-negative histiocytes. Cardiac involvement of RDD is rare. We report here an autopsy case of cardiac involvement of RDD presenting as fibrinous pericarditis. A 14-year-old Japanese boy complained of loss of appetite and breathing difficulty when lying down. He was found dead on his back in his bedroom. One year before his death, he was diagnosed with RDD after skin biopsy. At autopsy, the deceased was 153 cm in height and weighed 38 kg with systemic edema. He had flat pigmented light-brown spots, as well as many pale reddish-brown papules on the abdomen and both thighs. Cervical and mediastinal lymphadenopathy was observed. A large amount of pleural and ascitic fluid was observed. The spleen weighed 381.9 g and showed splenomegaly. The heart weighed 620 g and showed acute fibrinous pericarditis with adhesion. Abundant fibrin was observed on the epicardial surface. The infiltrating cells were CD68-positive, S100-positive, and CD1a-negative histiocytes. The skin and spleen showed histiocytic involvement. Systemic edema, large amounts of pleural and ascitic fluid, a high brain natriuretic peptide level in blood, and hemosiderin-laden macrophages in the lungs suggested chronic heart failure. We speculate that the cause of death was extranodal cardiac involvement of RDD with chronic heart failure. This case highlights the need for forensic pathologists to perform a complete autopsy to determine the cause of sudden death when cardiac involvement of RDD is present.     

Multiphasic cardiac magnetic resonance imaging: normal regional left ventricular wall thickening

Magnetic resonance imaging (MRI) is a completely noninvasive method for visualizing cardiovascular anatomy but has had limited use for assessment of cardiac function. The authors evaluated the use of gated MRI for the quantification of regional myocardial contraction. Nine normal subjects underwent gated MRI of five transverse sections (7 mm thickness) through the left ventricle at five intervals in the cardiac cycle using a new technique called rotating gated sequence. All five sections were examined, and the section that best demonstrated the midportion of the left ventricle in its maximum dimension was used to obtain measurement. This technique permitted assessment of regional wall thickening of various regions of the left ventricle in different phases of the cardiac cycle. The extent and percentage of wall thickening were calculated from measurements of the septum and anterior and lateral left ventricular wall in end-diastole and end-systole. The calculated mean values for extent and percentage of wall thickening for the septum were 0.40 cm and 40%; for the anterior wall, 0.61 cm and 73%; and for the lateral wall, 0.53 cm and 57%, respectively. A limitation of the current technique in wall thickness measurements is that the transverse MR plane of section is not perpendicular to the long axis of the left ventricle. Consequently, such oblique sections through the left ventricle may give inaccurate absolute wall thickness measurements but can provide reliable estimate of regional wall thickening dynamics. The ability to define left ventricular wall thickness and function without contrast media provides a noninvasive technique for the detection of segmental left ventricular myocardial dysfunction in ischemic heart disease.     

Simultaneous measurement of blood and myocardial velocity in the rat heart by phase contrast MRI using sparse q-space sampling

PURPOSE: To measure cardiac blood flow patterns and ventricular wall velocities through the cardiac cycle in anesthetized Wistar Kyoto (WKY) rats. MATERIALS AND METHODS: A gradient-echo cine pulse sequence incorporating pulsed field gradients (PFGs) provided phase contrast (PC) motion encoding. We achieved a range of velocity sensitivity that was sufficient to measure simultaneously the large flow velocities within the cardiac chambers and aortic outflow tract (up to 70 cm s(-1) during systole), and the comparatively small velocities of the cardiac wall (0-3 cm s(-1)). A scheme of sparsely sampling q-space combined with a probability-based method of velocity calculation permitted such measurements along three orthogonal axes, and yielded velocity vector maps in all four chambers of the heart and the aorta, in both longitudinal and transverse sections, for up to 12 time-points in the cardiac cycle. RESULTS: Left ventricular systole was associated with a symmetrical laminar flow pattern along the cardiac axis, with no appearance of turbulence. In contrast, blood showed a swirling motion within the right ventricle (RV) in the region of the pulmonary outflow tract. During left ventricular diastole a plume of blood entered the left ventricle (LV) from the left atrium. The ventricular flow patterns could also be correlated with measurements of left ventricular wall motion. The greatest velocities of the ventricular walls occurred in the transverse cardiac plane and were maximal during diastolic refilling. The cardiac wall motion in the longitudinal axis demonstrated a caudal-apical movement that may also contribute to diastolic refilling. CONCLUSION: The successful measurements of blood and myocardial velocity during normal myocardial function may be extended to quantify pathological cardiac changes in animal models of human cardiac disease.     

A case of delayed shock due to dissection of the hyperplastic coronary artery after balloon angioplasty and stenting

A 42-year-old obese woman with a history of liver cirrhosis and diabetes mellitus was admitted because of chest pain. Coronary balloon angioplasty and stenting were performed on the left anterior descending artery (LAD), which was 90% stenotic. She developed moderate shock about 6h later, and about 15 h after the procedure, she died from excessive bleeding from the right femoral artery because of removal of the catheter sheath by herself. Autopsy disclosed haemorrhagic cardiac tamponade and extensive haemorrhage into the epicardial adipose tissue, however, neither coronary perforation nor myocardial rupture was recognized. Histological examination of the dilated coronary segment revealed extensive dissection with an eccentric intimal thickening and the disruption of the adventitia. It was thought to be the origin of the haemorrhage. Although coronary dissection is a well-known complication during cardiac catheterization procedures, this report describes a rare fatal case with delayed onset of shock due to coronary dissection caused by balloon angioplasty and stenting in the presence of eccentric hyperplasia of the vessel wall.