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An enlarged heart can cause electrical instability and impaired contractility, leading to fatal arrhythmia and acute heart failure, and is associated with sudden cardiac death. However, there is limited postmortem evidence on whether heart weight is an independent factor associated with sudden cardiac death. This 18-month retrospective study examined 108 adult heart weights in which all the hearts were weighed after dissection, blood and blood clots removed, rinsed in water, and pat dried. The multivariate logistic regression analysis showed heart weight was an independent factor associated with sudden cardiac death. However, after normalization, the heart weight was a poor predictor of sudden cardiac death with an area under the curve less than 0.7 in the plotted receiver operating characteristic curve.

BACKGROUND Interrupted aortic arch (IAA) is a rare congenital heart disease defined by an interruption of the lumen and anatomical continuity between the ascending and descending major arteries. It is usually found within a few hours or days of birth. Without surgery, the chances of survival are low. If IAA patients have an effective collateral circulation established, they can survive into adulthood. However, IAA in adults is extremely rare, with few reported cases. CASE SUMMARY A 27-year-old woman presented with a 6-year history of progressively worsening shortness of breath and chest tightness on exertion. She had cyanotic lips and clubbing of the fingers. A transthoracic echocardiogram revealed an enlarged heart and dilation of the main pulmonary artery. There was an abnormal 9 mm passage between the descending aorta and pulmonary artery. The ventricular septal outflow tract had a 14 mm defect. Doppler ultrasound suggested a patent ductus arteriosus and computed tomographic angiography showed the absence of the aortic arch. The diagnoses were ventricular septal defect, patent ductus arteriosus, and definite interruption of the aortic arch. Although surgical correction was recommended, the patient declined due to the surgical risks and was treated with medications to reduce pulmonary artery pressure and treat heart failure. Her condition has been stable for 12 mo of follow-up. CONCLUSION Although rare, IAA should be considered in adults with refractory hypertension or unexplained congestive heart failure.

Myocarditis is an infectious–inflammatory disease with viral infections being one of the most common infectious cause. When it is superimposed to an individual genetic background, myocarditis may progress into a chronic heart muscle disorder, most often dilated cardiomyopathy (DCM), with a natural history similar to classic forms of genetic or idiopathic dilated cardiomyopathies. We present the case of a 30-year-old patient, with a persistent infectious episode in the last 8 weeks, pain and swelling in the large joints. At admission the patient had fever, tachycardia and a grade 2/6 systolic mitral murmur. Laboratory findings revealed inflammatory syndrome, hepatocytolysis syndrome and microalbuminuria. The electrocardiogram (ECG) showed possible right atrial tachycardia. The echocardiography revealed a globally enlarged heart with reduced ejection fraction and diffuse hypokinesia. When discussing the etiology of the DCM, the following were taken into consideration: a tachycardiomyopathy, ischemic etiology, genetic component, autoimmune etiology (elevated anti-Ro titer), and myocarditis. The diagnosis of myocarditis was confirmed by the cardiac magnetic resonance imaging which showed diffuse fibrosis of the interstitial space and an important increase of the extracellular volume. This case is distinguished by a particular immunological panel requiring dynamic monitoring in order to diagnose a possible associated autoimmune pathology.

A 69-year-old woman with previous pancreaticoduodenectomy was admitted for evaluation of chest discomfort on effort and leg edema for a few months. Oral flosemide before admission for 1 week failed to relieve her symptoms. Her blood pressure was 105/51 mmHg and heart rate was 76 beats/min. Chest X-ray revealed an enlarged heart and mild pulmonary congestion. Echocardiography demonstrated normal left ventricular ejection fraction and diastolic dysfunction with no left ventricular hypertrophy. Cardiac catheterization showed normal coronary arteries, high cardiac index, and elevated intracardial pressures. Myocardial biopsy from the right ventricular septum revealed nearly normal findings. Cardiac magnetic resonance imaging (CMRI) showed both ventricles enlarged and increased global extracellular volume fraction (ECV) of 37%, but normal native T1 and T2 values. As she had pancreaticoduodenectomy, beriberi was suspected. Vitamin B1 significantly increased urine output and lowered intracardiac pressures and cardiac index. After 3 months of vitamin B1, CMRI exhibited that the right ventricle had decreased in size and the global ECV value had been lowered. Our case highlights that chronic beriberi may be associated with little myocardial damage. The increased ECV suggests that the diffuse expansion of extracellular space unrelated to myocardial edema might have been reversed by vitamin B1treatment. Morphological changes in the ventricles and myocardial damage by wet beriberi can be demonstrated by CMRI.

An 87-year-old patient donated his body to the Institute of Anatomy and Cell Biology in gratefulness for the longevity of a Bjork-Shiley convexo-concave (BSCC) prosthetic aortic valve, implanted 34 years ago. The dissection of the enlarged heart showed no major signs of thrombosis, malignant fibrosis, or any other relevant issue that could potentially lead to valve failure as in other patients. Despite the reported high mortality rate of the earlier designs, especially of the BSCC valves, some patients survived for longer than expected. In more than 34 years after the BSCC valve implantation, the patient was a very active and lively man, working both as full-time and volunteer firefighter. The lifespan of this BSCC valve is among the longest reported.

OBJECTIVE: Functional mitral regurgitation in the setting of an enlarged heart is challenging to repair surgically with an annular approach, and the need to develop sub-annular and ventricular approaches is recognized yet unrealized due to the lack of models for investigations. In this study, we report a novel model of functional mitral regurgitation induced by left ventricular thinning and distension in pig hearts. METHODS: Seven pig hearts were explanted at a local slaughterhouse, and left ventricular distension induced by thinning the ventricular myocardium by 60–65% of its original thickness. Distension of the thinned hearts with a 120mmHg column, confirmed significant left ventricular dilatation and mitral valve tethering. These hearts were then mounted into a pulsatile flow model, and animated at 120mm Hg left ventricular pressure, 5L/min cardiac output at 70 beats per minute. Echocardiography was used to assess valvular kinematics and hemodynamics. RESULTS: Left ventricular wall thickness reduced by 60.5±10.1% at the basal plane, 64.8±11.3% at the equatorial plane and 64.0±11.4% at the apical plane after thinning. Upon distension, ventricular volumes increased by 852.4±639.8% after LV thinning, with an 89.5±33.9% increase in sphericity index. Mitral valve systolic tenting height increased from 7.92±2.06 mm to 15.02±3.89 mm, systolic tethering area increased from 130.7±38.2 mm(2) to 409.9±124.6 mm(2) and an average mitral regurgitation fraction of 24.4±16.6% was measured. In a case study, use of multi-modality imaging to test the efficacy of transcatheter mitral devices was confirmed. CONCLUSIONS: Ventricular wall thinning leading to passive left ventricular distension and dilatation is a reproducible ex vivo model of mitral valve tethering and functional mitral regurgitation, which in combination with multi-modality imaging provides a good simulation model.

Peripartum cardiomyopathy is a relatively rare condition, that usually presents with features of heart failure in the peripartum period. The ongoing pandemic caused by coronavirus disease 2019 (COVID-19) has been reported to be associated with myocarditis, with progression to dilated cardiomyopathy and heart failure. Dilated cardiomyopathy in a peripartum patient with COVID-19 infection may present a diagnostic dilemma. We report a case of dilated cardiomyopathy in a peripartum patient with COVID-19 infection. She presented with shortness of breath in the peripartum period. Chest X-ray showed a grossly enlarged heart with bilateral pulmonary infiltrates consistent with congestive heart failure or viral pneumonia. Echocardiography revealed dilated chambers with 22% left ventricular ejection fraction (LVEF) and global hypokinesis. Despite completing 5 days of remdesivir and dexamethasone, she had worsening dyspnea on postpartum day 10, a repeat echocardiogram showed further reduction in LVEF to 10-15% and was discharged with a life-vest after acute management. She had multiple hospital admissions for decompensated heart failure. Myocardial core biopsy showed marked acute inflammation and necrosis. She had an intra-aortic balloon pump, left ventricular and right ventricular assist devices placed on account of persistent hemodynamic instability, and is now scheduled to have a cardiac transplant.

Introduction: Presence of an enlarged heart provides a basis for determination of the cause and mechanisms of death. Gender, physical activity, and Body Mass Index (BMI) may affect the sizeof organs. Knowledge on such normal variations is needed in order to recognize theabnormalities.Objectives- This research was conducted to study the dimensions of the heart(heart weight, left ventricular thickness and valvular circumferences) among the young adult healthy deceased autopsies and evaluate their association with differentvariables.Methods: It was a descriptive cross-sectional study and 20-40 years of age healthy, young, adult, males and females in equal numbers who had died suddenly were studied by considering the inclusion and exclusion criteria. Details of the past history and the measurements were enteredinto a proforma and the anonymous data wereused for analysis.Results: The study revealed that the mean values of the heartweight was 280.52g (SD+/- 42.60), it was 293.94g (SD+/-39.29) for males and 267.10g (SD+/-42.64) for females. There was no significant association of heart weight with gender (P= 0.46410). There was a significant association between BMI and the heart weight of the females (P= 0.0387), no such association for left ventricular wall thickness. Further, there was a significant difference of the tricuspid valve circumference among two genders and the values were 11.6cm (SD+/-0.82) for males and 10.7cm (SD+/-0.6) forfemales.Conclusions: Majority of the findings was consistent with the findings of the studies globally on Caucasians. Increased body mass index was significantly associated with increased heart weight among females which could probably be explained as a consequence of increased epicardial fat since there was no such association for left ventricular wallthickness.

Right ventricular dysplasia (RVD) is a rare disease of the heart that primarily affects the right ventricle. It is a clinical and pathological entity that presents classically with palpitations, syncope, or even sudden death. It presents rarely in the elderly. Where sudden death is the first and only presentation, an autopsy is required to make the diagnosis. However, the pathomorphological features of RVD can easily be overlooked or missed at autopsy. We report the case of a 68-year-old male with the past medical history of hypertension, gout and inflammatory bowel syndrome. He was admitted on account of difficulty in breathing, abdominal swelling and reduced urination. Physical examination revealed hypertension with cardiac murmurs, widespread crepitations, distended abdomen and lower limb oedema. Provisional diagnoses of acute-on-chronic kidney disease and congestive cardiac failure secondary to hypertensive heart disease, precipitated by probable gastrointestinal infection were made. While on admission, he had an episode of syncope. Electrocardiogram revealed bigeminy and bradycardic sinus rhythm with unifocal ventricular premature contraction. He died on the 8thweek of admission. Autopsy revealed an enlarged heart weighing 600gm; there was thinning of the apical aspect of the right ventricular wall with subtotal fibrofatty replacement. Microscopic examination revealed a transmural replacement of cardiac myocytes by fibroadipose tissue extending inwards, in the most parts, from the epicardium to the endocardial surface. Our aim is to increase the awareness of these pathomorphological features among anatomic/forensic pathologists.

Simple Summary Cardiac diseases are a common finding in captive parrots. In this retrospective study, the cardiac silhouette of 36 wild galahs was measured in the ventrodorsal and laterolateral projections using radiographic images. The aim of the study was to determine reference values of the width and the length of the heart of wild galahs in relation to other anatomic landmarks. The evaluated reference indicates that the width of the heart is 50–65% of the thoracic width and 570–743% of the coracoid width. Abstract Background: Part of the diagnostic workup for cardiac diseases is radiographic imaging. To determine an enlarged heart, species-specific reference values are necessary. Wild birds are rarely diagnosed with cardiac disease, and only a few studies have been done to investigate the cardiac silhouette in wild birds. Methods: In this retrospective study, the cardiac silhouette of 36 wild galahs, presented at the hospital, was investigated in relation to other anatomic landmarks like the thoracic width, clavicula width, synsacrum width, distance between the third and fourth rib, distance of the clavicula, and length and height of the sternum using a digital DICOM viewer. Results: The cardiac width was significant compared to the thoracic width with a minimum to maximum of 50 to 65%. The cardiac width compared with the coracoid width also showed significant results with a minimum to maximum range of 570 to 743%. A significant correlation was found between the weight and the cardiac width and length. Conclusion: The cardiac silhouette in wild galahs is easily measured in both radiographic views, and the heart size can be compared to other anatomical landmarks.

Dextrocardia is a rare congenital cardiac positional anomaly. A 74-year-old woman was referred for aortic regurgitation (AR). Chest X-ray revealed a mildly enlarged heart that directed to the right side. Transthoracic echocardiography showed AR due to cusp prolapse with a dilated left ventricle and reduced wall motion. Computed tomography demonstrated the heart and great vessels in a mirror image of their normal positions. A median sternotomy performed by the surgeon standing on the right side of the patient. After establishing a cardiopulmonary bypass, the surgeon moved to the left side of the patient, and then performed aortic valve replacement.

Cardiology was called to review a neonate with cyanosis at 6 hours of life. The oxygen saturations averaged 70% at baseline with no preductal and postductal difference. No cardiac murmurs were heard, but the chest X-ray showed an enlarged heart. Transthoracic echocardiography (TTE) demonstrated a small patent arterial duct and a patent oval foramen, both with left-to-right flow across. TTE also showed dilatation of the left atrium (LA) and left ventricle (LV) (figure 1A), suggesting increased flow to the left—heart (figure 1B). The atrioventricular and ventriculoarterial connections were normal. Figure 1 Image panel outlining the diagnostic approach to the echocardiographic evaluation of the patient. …

Cardiac biomarkers are important tools for monitoring disease progress and can monitor progression of therapy. Endothelin-1 (ET-1) has been studied for its use as a cardiac biomarker in human and small animal medicine while in horses with cardiac disease it has not been evaluated yet. The objective of the present study was to determine the concentration of plasma ET-1 in healthy horses and compare it with ET-1 concentration in horses with cardiac disease during rest and after exercise. Fifty four horses admitted to the Equine Clinic of Free University of Berlin were used in the present study, of which 15 horses were clinically healthy with no evidence of cardiac disease (Group 1), 22 horses suffered from cardiac disease with normal heart dimensions (Group 2) and 17 horses with cardiac disease and enlarged heart diameters (Group 3). Clinical examination, electrocardiography and echocardiography were performed. Endothelin-1 concentration was determined using ET-1 ELISA kit. The concentration of plasma ET-1 was significantly increased in horses with cardiac disease and normal cardiac dimensions (Group 2) and in horses with cardiac disease and enlargement of the left atrium (Group 3) compared to its concentration in clinically healthy horses (Group 1). In addition, the concentration of plasma ET-1 after exercise was significantly increased in diseased horses compared to its concentration at rest. Detection of ET-1 plasma concentration in horses at rest may be useful for detecting horses with changes in left atrial cardiac dimensions.

Old age is often attacked the cardiovascular diseases such as hypertension. Ministry of Health Republic of Indonesia (2012) states that hypertension is one of the most influential risk factors for the incidence of heart disease and blood vessels. High blood pressure continuously increases the burden of the arteries slowly. The arteries undergo hardening process becomes thick and rigid, thus reducing its elasticity. Hypertension can also lead to heart disease because if high blood pressure is left without regular treatment, the heart must pump very strongly to push blood into the arteries, over time the walls of the heart muscle become thicker. An abnormally enlarged heart is an unhealthy heart because the heart becomes stiff and the beat tends to be irregular. This will make pumping less effective and eventually lead to heart failure. Pharmacologic treatment using drugs have the risk of side effects. The purpose of this study was to analyze the effectiveness of laughter yoga as non-pharmacological therapy in the elderly with hypertension by measuring the difference in blood pressure before and after being treated laughter yoga. Quantitative experimental research with pretest-posttest with a control group design. The sample used purposive sampling that is 20 elderly that is 10 elderly with treatment and 10 elderly as a control. The instrument was used analog tensimeter. Wilxocon different test results obtained from pre-treatment group of post systole and diastole p-value 0,007 and 0,003. While in control group of pre-post systole and diastole p-value 0,831 and 0,084. Laughter yoga effectively against decreased blood pressure in the elderly with grade 2 hypertension at the Panti Wredha Salib Putih Salatiga.

Congenital muscular dystrophies (CMD) are a group of heterogeneous disorders. Here, targeted next generation sequencing of 168 CMD-associated genes was performed on collected clinic samples to identify potential mutations. A loss-of-function mutation (c.4676-4682delGCTGCAA; p.Cys1560Thrfs*33) of the LAMA2 gene in a consanguineous family was identified and confirmed by Sanger sequencing. The second recessive mutation in SYNE1 (c.2881C>T; p.Arg961Trp) was found in the SAP motif, which was predicted to be involved in chromosomal organization. The third homozygous mutation (c.32462C>T; p.Pro10821Leu) in TTN was mapped to the third PPAK motif of the encoded protein. Muscle biopsies of the proband showed large variations in muscle fiber size, necrotic and regenerating fibers and an increase in endomysial collagen tissue. To the best of our knowledge, this is the first case with CMD and mildly enlarged heart, carrying three novel recessive mutations in LAMA2, SYNE1, and TTN.

Background: Patient diagnosed with double inlet left ventricle (prevalent in 5 – 10 in 100,000 newborns) complicated with Eisenmenger syndrome had a median survival age of 14 years without corrective surgery. Congenital heart disease such as this is usually treated by multiple surgeries during early childhood. A surgically uncorrected case in adults is not of common occurrence. Further, generalized itching after coming in contact with water (aquagenic pruritis) presented an interesting conundrum to treat. Case: A 29-year-old patient in India presented at a primary health care center with a history of difficulty breathing and discoloration of extremities since birth. He also gave a history of itching which commonly occurred after taking bath, hemoptysis and history of turning blue in color after birth. Patient had received no treatment besides regular phlebotomies. On examination, there was grade IV clubbing and conjunctival congestion. Cardiovascular examination revealed an enlarged heart, heaving apex beat and a pan-systolic murmur. A provisional diagnosis of a congenital cyanotic heart disease was made. Investigations revealed hemoglobin of 16.8g/dl. X–ray and electrocardiogram showed hypertrophy of the ventricles. An echocardiogram showed double inlet left ventricle with L-malposed vessels but without pulmonary stenosis. A final diagnosis of congenital heart disease; double inlet left ventricle, L-malposed vessels without pulmonary stenosis, Eisenmenger Syndrome and absolute erythrocytosis was made. Patient was advised for further management with a cardiologist in a tertiary center but the patient did not follow up. Conclusion: Unlike in high-income countries where most congenital heart diseases are detected and dealt with at birth whereas low-and middle-income nations often have to deal with cases that present much later and should often be included in the differential diagnosis. Inability to follow up cases, centers that are poorly equipped and lack of facilities for investigations, patient’s lack of medical awareness, and financial restrictions are major barriers to providing optimal treatment.

The first description of the enlarged heart of athletes came in 1899, based only on physical examination with percussion, but later recognized by quantitative chest radiology [(1)][1]. Over the past 40 years, imaging (largely with echocardiography) has provided a direct assessment of “athlete’s

A 43-year-old man was referred to a nearby hospital because of exertional dyspnoea. Chest radiography revealed an enlarged heart and bilateral lower lung infiltrates (figure 1A). Chest CT revealed bilateral basal pulmonary consolidations, pericardial effusion and small amounts of pleural effusion bilaterally (figure 1B). He was referred to our hospital and underwent pericardiocentesis. Because of a high triglyceride concentration in the pericardial effusate (1287 mg/dL), the patient was diagnosed with chylopericardium. He was prescribed a low-fat diet with subsequent resolution of the pericardial effusion and exertional dyspnoea. Although the bilateral consolidations on chest CT also resolved (figure 1C), on the following year, ground-glass opacities appeared, mainly in the right upper lobe and right S6 (figure 1D). The patient’s physical examination and blood test results were unremarkable. His pulmonary function tests were normal. The findings of bronchoalveolar lavage fluid obtained from …

Hypertension is a major disease that affects millions of people world-wide. If hypertension remains untreated for long time it could give rise to an enlarged heart condition called Left Ventricular Hypertrophy (LVH). However, recent research in medical domain proposes that left ventricular diastolic dysfunction (LVDD) may be considered as a preceding indicator of LVH. The analysis of ECG signal has shown significant results in identifying LVDD condition that can lead to LVH, however the analysis method till date have remain limited to the manual examination of time domain features of ECG parameters by the experts which is time consuming and cumbersome. Since the time-frequency analysis of the ECG signal have shown more promising results in diagnosis of any abnormality related to the cardiac system, therefore the application of this method is employed in the patients suffering from hypertension and for assessment of the future risk(s) in developing LVH. In the study, we have proposed a Stockwell Transform based time-frequency analysis method of the ECG features (QRS Complex, P-Wave and T-Wave) for accessing the preceding stage of the myocardial remodeling phase. To perform the study, ECG features of the 60 subjects recorded from hospital comprising of 30 controlled and 30 hypertension cases were studied. At the location of the QRS interval a spreading in the power is observed in diseased patients, which signifies increased ventricular activation time, also the power level of the P-Wave and T-Wave have shown significant changes. Increased Ventricular activation time and P-Wave dispersion observed in the frequency domain along with P-wave terminal force, can be used as an indicator of associated risk of developing Left Ventricular Hypertrophy.

Background Several inherited cardiac diseases may lead to sudden cardiac death (SCD) a devastating event in the families. It is crucial to establish a post mortem diagnosis to facilitate relevant work-up and treatment of family members. Sudden unexplained death (SUD) victims constitute roughly one third of all SCD cases in Denmark. Methods This was a single center, retrospective study investigating SUD cases. Victims who died unexplained due to suspected or confirmed cardiac disease were consecutively referred to a third line referral center established in 2005. All autopsy reports were investigated. Victims were divided into two groups: non-diagnostic cardiac findings and normal cardiac findings. None of the included victims had findings consistent with a diagnosis based on existing criteria. Results In total, 99 SUD cases were referred. The mean age of the victims was 37 years (range 0–62 years, 75% males). A total of 14 (14%) victims had a cardiovascular diagnosis pre-mortem. Thirty-seven cases had normal cardiac findings and non-diagnostic cardiac findings were found in 62 cases (63%). The five most common findings included ventricular hypertrophy and/or enlarged heart (n = 35, 35%), coronary atheromatosis (n = 31, 31%), myocardial fibrosis (n = 19, 19%), dilated chambers (n = 7, 7%) and myocardial inflammation (n = 5, 5%). Conclusion One third of SUD victims had normal cardiac findings and non-diagnostic cardiac findings were seen in almost two thirds of the SUD victims. These non-diagnostic findings may be precursors or early markers for underlying structural cardiac disorders or may be innocent bystanders in some cases. Further studies and improved post-mortem examination methods are needed for optimization of diagnostics in SUD.

The aim of this study was to evaluate the reliability of the cardiothoracic ratio (CTR) in postmortem computed tomography (PMCT) and to assess a CTR threshold for the diagnosis of cardiomegaly based on the weight of the heart at autopsy. PMCT data of 170 deceased human adults were retrospectively evaluated by two blinded radiologists. The CTR was measured on axial computed tomography images and the actual cardiac weight was weighed at autopsy. Inter-rater reliability, sensitivity, and specificity were calculated. Receiver operating characteristic curves were calculated to assess enlarged heart weight by CTR. The autopsy definition of cardiomegaly was based on normal values of the Zeek method (within a range of both, one or two SD) and the Smith method (within the given range). Intra-class correlation coefficients demonstrated excellent agreements (0.983) regarding CTR measurements. In 105/170 (62 %) cases the CTR in PMCT was >0.5, indicating enlarged heart weight, according to clinical references. The mean heart weight measured in autopsy was 405 ± 105 g. As a result, 114/170 (67 %) cases were interpreted as having enlarged heart weights according to the normal values of Zeek within one SD, while 97/170 (57 %) were within two SD. 100/170 (59 %) were assessed as enlarged according to Smith's normal values. The sensitivity/specificity of the 0.5 cut-off of the CTR for the diagnosis of enlarged heart weight was 78/71 % (Zeek one SD), 74/55 % (Zeek two SD), and 76/59 % (Smith), respectively. The discriminative power between normal heart weight and cardiomegaly was 79, 73, and 74 % for the Zeek (1SD/2SD) and Smith methods respectively. Changing the CTR threshold to 0.57 resulted in a minimum specificity of 95 % for all three definitions of cardiomegaly. With a CTR threshold of 0.57, cardiomegaly can be identified with a very high specificity. This may be useful if PMCT is used by forensic pathologists as a screening tool for medico-legal autopsies.

Objective The objective of this article is to evaluate whether the area of the four-chamber view of the fetal heart computed from two orthogonal diameters could be used to screen for cardiac malformations. Methods Two hundred control fetuses were examined between 20 and 40 weeks of gestation. The end-diastolic area was computed from the orthogonal basal-apical and transverse diameters obtained from the four-chamber view. Regression analysis of the computed area versus six independent variables was performed between 20 and 40 weeks. Fetuses with major heart defects were identified from a low-risk population of 4352 fetuses undergoing second-trimester or third-trimester screening ultrasound. The end-diastolic area was derived and the Z-score and centile computed. An area greater than the 95th centile was considered to be abnormal. Results From the screening population, the incidence of major heart defects was 2.8/1000. Of the 12 fetuses with major heart defects, 50% (6/12) demonstrated an area greater than the 95th centile. Of the fetuses with an enlarged heart, 66% (4/6) had outflow tract abnormalities. Conclusions Measurements of the orthogonal basal-apical and transverse diameters can be used to compute the area of the four-chamber view. Fetuses with major heart defects who have an enlarged heart can be identified using this technique. © 2016 John Wiley & Sons, Ltd.

The study assessed trends in posthypoxic changes in the cardiovascular system over the first six months of life in babies with and without fetal growth restriction. The infants born with fetal growth restriction and those born without this condition were found to have similar posthypoxic changes in terms of the type of dilated, hypertrophic cardiopathy or cardiopathy with normal heart chambers. The formation of normal heart function that remained during the first six months of life was impaired in all cases. Fetal growth restriction in babies with the lower heart chambers was related to the changes at birth and during 6 months of life, which were similar to those of cardiopathy with normal heart chambers, but more pronounced. Fetal growth restriction in infants with the enlarged heart chambers was associated with autonomic dysregulation as excessive sympathetic activity at birth, impaired automatism and conductivity, and decreased contractility and relaxation of the left ventricle. The sympathetic component and compensatory resources were observed to be depleted in these babies at the age of 6 months. More pronounced changes were associated with the duration and severity of fetal distress.

A 92-year-old woman was admitted to hospital for dyspnoea. She was diagnosed for the first time with congestive heart failure. Her medical history included hypertension and diabetes. Chest radiography and electrocardiography revealed an enlarged heart and paroxysmal atrial fibrillation, respectively

Metabolism research has seen a great burst of popularity in recent years: scientists and doctors are investigating its role not just in obesity and diabetes mellitus but also in cancer growth and heart disease. There was a time though, not so long ago, when the field was distinctly out of fashion. The basic biochemical mechanisms had been defined decades earlier, and researchers thought that metabolites had little more to offer. But for a select group of dedicated researchers, like Rong Tian, Director of the Mitochondria and Metabolism Center at the University of Washington, numerous questions remained unanswered. At a time when it was decidedly unpopular, Tian focused her research on understanding how metabolism affects heart function. What she found has come to challenge our assumptions about how simple sugar, fat, and amino acids affect the body. More than just energy sources, Tian has produced evidence that these molecules act as signals, changing the way cells behave in critically important ways.1–3 The heart consumes a tremendous amount of energy—at least 12× its weight in adenosine triphosphate each day. In healthy adults, fatty acids feed the heart, but glucose is the preferred energy source for both healthy fetal hearts and diseased adult hearts. Scientists have long wondered why the heart switches from one energy source to another. Tian found that neither substrate is toxic: the heart can be forced to use glucose or fatty acids with no ill effects. Rather, it is the flexibility to choose between the 2 sources that is essential.4–6 Rong Tian Tian’s work has also contributed to our understanding of metabolic cardiomyopathy.7–9 A cellular energy sensor, known as adenosine monophosphate–activated kinase, is also a master regulator of metabolism. Mutations in the kinase result in an enlarged heart with arrhythmia, …

A captive, 22-year-old, intact male Sunda wrinkled hornbill (Aceros corrugatus) was presented for an acute onset of open-mouth breathing and bilaterally drooped wings. An external physical examination revealed a moderately thin body condition, marked respiratory effort, and a significant heart murmur. Diagnostic blood testing revealed moderate azotemia and persistent erythrocytosis, initially documented 2 years before this event. Radiographic imaging revealed a subjectively enlarged heart and a right dorsal coelomic cavity mass. Further diagnostic testing included an echocardiogram and ultrasound-guided fine-needle aspirate of the right coelomic cavity mass, with cytology consistent with a carcinoma. The bird was euthanatized because of the poor prognosis. Necropsy and histopathology identified right atrioventricular valve hypertrophy with severe hypertrophic and dilated cardiomyopathy of the right ventricular free wall, atherosclerosis of the great vessels and arteriosclerosis of myocardial vessels, severe hepatic extramedullary hematopoiesis, and pulmonary carcinoma of the right lung. In this case, erythrocytosis was considered a physiologic response to hypoxemia caused by the lung mass.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease, often familial, characterized pathologically by fibrofatty replacement of the right ventricular myocardium, resulting in thinning of the ventricle. ARVC is an important cause of sudden death in individuals less than 30 years of age and has been found in up to 20% of sudden deaths in young people. A 21-year-old male collapsed to the ground while playing with his friends for about 10 minutes time. There was no history of trauma prior to the collapse. He had a mild upper respiratory tract infection three days prior, however he was not on any medication at the time of this incident. He was immediately taken to the nearby hospital where he was found to be in cardiac arrest. Post-mortem examination revealed an enlarged heart (heart weight 545 g). The right ventricular wall thickness was 6 mm. Coronary arteries were normal in configuration with a left dominant circulation. The right and left coronary ostiae were patent. Coronaries were free from atherosclerotic narrowing. Sections from the right ventricular myocardium showed variable, predominantly epicardial fibrosis throughout and transmural infiltration of adipocytes. The cardiomyocytes in these areas showed patchy vacuolation and nuclear hypertrophy. The remaining myocardium was mainly unremarkable. These findings were in keeping with arrythmogenic right ventricular cardiomyopathy. The importance of a thorough knowledge on specific cardiac conditions that can lead to sudden death and the importance in thorough sampling of cardiac muscle in such cases is highlighted here.

Sarcoidosis is a granulomatous disease of unknown etiology, which can affect people of all racial and ethnic groups and can occur at all ages. Currently, sarcoidosis is considered as a worldwide disease with different prevalence rates. Arrhythmias are the leading cause of sudden death among patients diagnosed with cardiac sarcoidosis. In this case, the deceased was a 51-year-old male, a foreigner, with a history of type II diabetes and hypertension and was on treatment for 12 years. He was found unresponsive in a chair at his residence by his son. Autopsy revealed an enlarged heart (heart weight 543 g, 95th percentile for height is 387 g; 95th percentile for weight is 474 g). The pericardial sac is intact. There are no adhesions and no collections of fluid or blood. Epicardium was unremarkable. No acute ischaemic changes were seen in the myocardium. The coronary arteries were normal in configuration with a right dominant circulation. Histopathology of all organs were performed. Sections of myocardium showed varying degrees of replacement fibrosis with an inflammatory infiltrate comprising epithelioid histiocytes, giant cells and occasional non-necrotizing granulomata. There were no acute ischaemic changes. Toxicology screening was negative for common poisons and substance of abuse. These findings were in keeping with cardiac sarcoidosis and concluded it as cause of death. This was a rare case of sarcoidosis where the diagnosis was made with the aid of thorough histopathology examination. The importance of a thorough knowledge on specific cardiac conditions that can cause sudden death is highlighted here.

Objectives Endoglin is a co-receptor for TGFbeta/BMP9/10 signalling and ENG mutations lead to the vascular disorder hereditary haemorrhagic telangiectasia type I (HHT). Endoglin is also required for normal vascular development and angiogenesis, but little is known about endoglin’s role in quiescent adult vascular endothelium. Methods To investigate this role, tamoxifen was administered to adult Cdh5(PAC)-CreERT2;Engfl/fl mice to generate endothelial-specific depletion of endoglin (Eng-iKOe). Cardiac magnetic resonance imaging, myography, vascular casting, microsphere injection, immunohistology, qPCR and aortic telemetry were used to evaluate cardiovascular changes after endoglin knockdown. Results Endothelial-specific loss of endoglin leads to an enlarged heart and cardiomyocyte hypertrophy within 5 weeks, progressing to high output heart failure (HOHF). In vivo aortic telemetry revealed significant loss of aortic pressure within a few days of endoglin depletion. Increased cardiac size and reduced cardiac afterload were confirmed by ventricular pressure loop analysis. As HOHF could result from arteriovenous malformations (AVMs), and these are found primarily in mucocutaneous and pulmonary tissues in HHT, we systematically screened for AVMs using microspheres and vascular casting. Although AVMs were absent in the majority of tissues, they were observed in the pelvic region and may account for the rapid increase in cardiac output. Having also observed an increase of VEGF-A protein in tissues from Eng-iKOe mice, we found that inhibition of VEGFR2 was protective against enlargement of the heart and dilatation of the ventricles. Conclusion Our results showed the essential role of endoglin in the maintenance of adult cardiovasculature through crosstalk with the VEGF signalling pathway.

Purpose Automated pulmonary embolism (PE) segmentation is frequently used as a preprocessing step in the quantitative analysis of pulmonary embolism. Objective of this study is to analyze the potential limitation in automated PE segmentation using clinical cases. Methods A database of 304 computer tomography pulmonary angiography (CTPA) examinations was collected and confirmed to be PE. After processing using an automated scheme, two radiologists classified these cases into four groups of A, B, C and D, which represent 4 different segmentation results namely, (1) entire pulmonary artery identified without motivation artifacts, (2) entire pulmonary artery identified with motivation artifacts, (3) part of the pulmonary artery identified, and (4) none of the pulmonary artery identified. Then, the possible failed reasons in PE segmentation were analyzed and determined based on the image characterization of the diseases and the applied CTPA scanning protocols. Results In the study, 143 (47.0%., 30 (9.9%., 110 (36.2%. and 21 (6.9%. examinations were classified into groups A, B, C and D, respectively. Group C and D included the cases with failed segmentation. Fifteen failure reasons, including intrapulmonary abnormalities, extra-pulmonary abnormalities, diffuse pulmonary diseases, enlarged heart, absolute occluded vessels, embolism attached to artery wall, delayed scan time, skewed location, low scan dose, obvious artifact of superior vena cava, previous chest surgery, congenital deformities of the chest, incorrect positioning, missed images and other unknown reasons, were determined with corresponding case percentages ranging from 0.3%.o 9.2%. Conclusions Automated segmentation failures were caused by specific lung diseases, anatomy varieties, improper scan time, improper scan dose, manual errors or other unknown reasons. Realization of those limitations is crucial for developing robust automated schemes to handle these issues in a single pass when a large number of CTPA examinations need to be analyzed.

It is common for patients with rheumatic heart disease to have an enlarged heart. We investigated the prognostic value of cardiothoracic ratio (CTR) in patients with rheumatic heart disease undergoing valve replacement surgery.A total of 1772 patients were divided into 4 groups based on the quartiles of preoperative CTR:0.56 (n = 349), 0.56-0.61 (n = 488), 0.61-0.66 (n = 449) and ≥0.66 (n = 486). The CTR was measured from postero-anterior chest radiographs. We then investigated the association between the CTR and adverse outcomes.In-hospital mortality was 4.0% (71/1772). Analyses of receiver operating characteristic curves showed that, at a cut-off of 0.6, the CTR exhibited 66.2% sensitivity and 64.0% specificity for detecting in-hospital death (area under curve 0.671, P 0.001). The prevalence of in-hospital death was 7.1% in males with a CTR0.6, which was significantly higher in males without a CTR. A similar result was observed in females (1.9 vs 5.1%, P = 0.004). Multivariable regression showed that a CTR0.6 was an independent predictor of in-hospital (odds ratio 2.36, P = 0.005) and 1-year mortality (hazard ratio 2.06, P = 0.006). Kaplan-Meier curves, for the cumulative rate of 1-year mortality among groups, indicated that the risk of death was increased if the CTR0.6 (log-rank 16.36, P 0.001).CTR, as a simple and reproducible indicator, was identified as a prognostic factor for predicting poor outcomes in patients with rheumatic heart disease undergoing valve replacement surgery.

Background Pediatric dilated cardiomyopathy (DCM) is associated with death or transplantation and is typically considered a homogeneous process affecting global left ventricular (LV) function. However, assessment of regional abnormalities that contribute to pumping inefficiencies is lacking. The aim of this study was to define regional strain patterns of mechanical inefficiency in the broader context of LV discoordination (dysfunction and timing abnormalities) and to evaluate their associations with LV function and clinical outcomes. Methods Multiplanar apical LV echocardiographic images from patients with pediatric DCM ( n = 56) and control subjects ( n = 20) were analyzed by two-dimensional longitudinal speckle-tracking strain analysis to identify segmental strain patterns and global contraction groups. Clinical outcome (death or transplantation vs transplantation-free survival) and echocardiographic data were evaluated. Outcome groups were compared using the Fisher exact test, the χ 2 test, or analysis of variance (with P values ≤ .05 considered to indicate statistical significance). Results Of 56 patients with DCM, 29 (52%) progressed to death or transplantation. Five segmental strain patterns were observed that were used to define seven contraction groups by regional contractility and/or timing discoordination. The group(s) with the most discoordination had the most LV dysfunction ( P = .0004) and a trend toward the highest frequency of death or transplantation ( P = .069). Interreader reproducibility of segmental strain patterns agreed in 165 or 180 (92%) segments tested (κ = 0.90). Control subjects had normal strain patterns. Conclusions A heterogeneous mixture of abnormalities in the regional wall mechanics that lead to inefficient pump mechanics through functional and timing abnormalities were seen in this cohort and were categorized into natural subgroups. More severe LV discoordination was associated with increased LV dysfunction and a trend toward death or transplantation.

Background Rat developmental toxicity including embryolethality and teratogenicity (mainly ventricular septal defects [VSDs] and wavy ribs) was produced by an N-phenylimide herbicide that inhibits protoporphyrinogen oxidase (PPO) common to chlorophyll and heme biosynthesis. Major characteristics of the developmental toxicity included species difference between rats and rabbits, compound-specific difference among structurally similar herbicides, and sensitive period. Protoporphyrin accumulation in treated fetuses closely correlated with the major characteristics. Iron deposits in erythroblastic mitochondria and degeneration of erythroblasts were observed in treated rat fetuses. In this study we investigated fetal anemia and subsequent developmental effects in rats, and inhibition of PPO in rats, rabbits, and humans by the herbicides in vitro. Methods Fetuses were treated on gestational day (GD) 12 and removed on GDs 13 through 20. All litters were examined externally. One half of litters were examined for blood and skeletal development, and the other half for interventricular foramen closure. Effects on PPO were determined in mitochondria from embryos and adult livers. Results Fetal anemia in rats was evident on GDs 13 through 16. Subsequently, enlarged heart, delayed closure of the foramen, reduced serum protein, and retarded rib ossification were observed. In vitro PPO inhibition exhibited species- and compound-specific differences corresponding to the developmental toxicity. Conclusion We propose that developmental toxicity results from PPO inhibition in primitive erythroblasts, causing transient fetal anemia followed by death. Compensatory enlargement of the fetal heart results in failure of interventricular foramen closure and VSD. Reduced serum protein leads to delayed ossification and wavy ribs

History A 61-year-old man with no relevant medical history was admitted to the emergency department with symptoms of congestive heart failure and a 1-week history of chest pain, progressive dyspnea, abdominal swelling, bipedal edema, and anorexia. Laboratory test results, including complete blood count and electrolyte, creatinine, creatine phosphokinase, and troponin T levels were normal. Electrocardiographic findings were unremarkable. Initial chest radiography showed an enlarged heart with bilateral pleural effusion. Transthoracic echocardiography revealed an irregular right atrial mass and moderate to severe pericardial effusion. The patient subsequently underwent computed tomography (CT) of the chest, abdomen, and pelvis followed by cardiac magnetic resonance (MR) imaging for further evaluation of the atrial mass. Because of the suspected diagnosis, conventional radiography of the skeleton was performed.

The postnatal period in preterm infants involves multiple physiologic changes starting directly after birth and continuing for days or weeks. To recognize and treat compromise, it is important to measure cardiovascular function. We used a novel technique (speckle tracking echocardiography, STE) to measure cardiac function in this period. We obtained cardiac ultrasound images at day 3, 7, 14, 21 and 28 in preterm infants

Selenium (Se) is a trace element playing an important role in animal and human physiological homeostasis. It is a key component in selenoproteins (SeP) exerting multiple actions on endocrine, immune, inflammatory and reproductive processes. The SeP family of glutathione peroxidases (GSH-Px) inactivates peroxides and thereby maintains physiological muscle function in humans and animals. Animals with high feed conversion efficiency and substantial muscle mass have shown susceptibility to Se deficiency related diseases since nutritional requirements of the organism may not be covered. Mulberry Heart Disease (MHD) in pigs is an important manifestation of Se deficiency often implicating acute heart failure and sudden death without prior clinical signs. Post-mortem findings include hemorrhagic and pale myocardial areas accompanied by fluid accumulation in the pericardial sac and pleural cavity. Challenges in MHD are emerging in various parts of the world. Se is of fundamental importance also to human health. In the 1930s the Se deficiency associated cardiomyopathy named Keshan Disease (KD) was described for the first time in China. Various manifestations, such as cardiogenic shock, enlarged heart, congestive heart failure, and cardiac arrhythmias are common. Multifocal necrosis and fibrous replacement of myocardium are characteristic findings. Pathological findings in MD and KD show striking similarities.

Sheffield Children’s Hospital, Sheffield A 7 month old baby seen in respiratory clinic following referral by local hospital for persistent chestiness and chronic lung collapse on CXR. He was born at 36 weeks, was well and thriving. He started with chesty cough and occasional grunting from 3 months of age, admitted at 4 months with bronchiolitis type illness, and reduced feeding. O/E had mild temperature (37.8), reduced air-entry on left lower lobe, and raised CRP of 73, CXR showed complete collapse/consolidation of left lung, over inflation of right lung with mediastinal shift. He made reasonable recovery after short course of iv antibiotics and physiotherapy. On follow up he continued to have mild respiratory distress, repeat X-rays showed persistent left lower lobe collapse. In view if this he was referred to respiratory for bronchoscopy. On respiratory review he was noted be intermittently grunting and reduced air-entry on left lung. Cardiac examination showed a soft systolic murmur (gr 2/6) along left upper sternal edge, femorals good volume, no organomegaly. Cardiac work up done, echo- showed severe dilated left heart, mitral regurgitation, severely impaired function and abnormal origin of left Coronary artery from Pulmonary artery. ECG- showed ST elevation, T wave inversion and Deep Q waves in lateral leads. CT showed complete collapse of left lung due to compression by the enlarged heart. He was urgently transferred to cardiac centre for repair of ALCAPA. What was thought to be a primary respiratory problem in this infant turned out to be a significant cardiac anomaly.

This dissertation aimed to find new treatments for cardiovascular diseases. Nitric oxide (NO) promotes cardiovascular health, and is produced by the endothelium. We showed that a novel drug promoted NO-producing enzyme in a healthy state, and could treat mice with enlarged heart due to high blood pressure. Additionally, recent studies suggest that stimulation of lymph vessel formation can prevent atherosclerotic plaque development. We found a new gene in human plaque tissue. We showed that this gene could promote the formation of lymph vessels in cell culture and in zebrafish embryos. This gene may represent a new therapy for atherosclerotic patients.

High prevalence of iron deficiency (ID) and cardiomyopathy have been observed in patients with end-stage kidney disease (ESKD). Our objective was to clarify associations between ID and cardiac remodeling in patients with ESKD.A cross-sectional study was conducted using 1974 Japanese patients with ESKD at the initiation of maintenance dialysis. Levels of hemoglobin (Hb), iron status, and cardiac enlargement as assessed by the cardiothoracic ratio (CTR) were determined immediately before the first hemodialysis session. Circulatory ID was defined as transferrin saturation (TSAT) 20%, and stored ID was defined as ferritin level100 ng/dL.The mean age was 67 years. Median CTR was 54.0%. The prevalence of circulatory and stored ID was found to be 38% and 34%, respectively. CTR was higher in patients with circulatory ID than in those without. Even in ESKD patients without overhydration, significant negative association was observed between TSAT and CTR. Higher odds ratios in parallel with higher CTR categories compared with the reference category of CTR45% were found in patients with TSAT20% on multinomial analysis, but ferritin did not show any significant associations. The odds ratio for CTR54% showed an upward trend in patients with TSAT20% (odds ratio: 1.3) and10% (odds ratio: 1.6) compared with the reference, even after adjusting for confounding variables such as Hb and ferritin. However, that phenomenon was eliminated by adding usage of an iron agent.Circulatory ID is closely associated with an enlarged heart independent of ferritin and Hb. Iron supplementation in the predialysis phase of chronic kidney disease may prevent cardiac remodeling independent of Hb level in patients chronic kidney disease.

This study aimed to demonstrate the capacity for noninvasive localisation and characterisation of myocardial infarction (MI) in vivo using a hemispherical photoacoustic imaging (PAI) system. MI remains a leading cause of morbidity and mortality worldwide. To enable optimal treatment of patients, timely and accurate diagnosis and longitudinal monitoring is critical. Ischaemia was induced in Balb/c mice by ligation of the left anterior descending artery. The hemispherical PAI system, equipped with 128 ultrasonic transducers spirally distributed on the surface, along with parallel data acquisition, was applied for imaging of the mouse heart. Our study showed that hemispherical PAI can delineate thoracic vessels and the morphology of the entire heart. Longitudinal PAI images revealed gradual expansion of the infarcted area along with necrosis and fibrosis, which were quantitatively validated by triphenyltetrazolium chloride staining. After MI modelling, the photoacoustic (PA) signal intensity decreased by 399.1 ± 56.3 (p

Dilated cardiomyopathy (DCMP) remains a life threatening disease in young patients and is often difficult to differentiate from myocarditis. Early recognition and treatment of DCMP are crucial for good prognoses in this patient population. The clinical course of patients with DCMP that result in cardiogenic shock varies according to the etiology as well as patient age. The volumetric expansion of the enlarged heart can compress adjacent structures causing a number of related symptoms, especially in infants with soft cartilaginous bronchi. Therapeutic strategies for treating these issues vary according to the type of complication encountered. We report a case of severe DCMP with sudden onset of massive cardiomegaly with heart failure complicated by bronchial obstruction in an infant.

A male Rio Grande Wild Turkey (Meleagris gallopavo intermedia) living in semidomestication was submitted for necropsy. Emaciation, a greatly enlarged heart, and chronic passive congestion of the liver were present. Dilated cardiomyopathy occurs in domestic turkey flocks but has not been reported in Wild Turkeys.

A one-year-old African pygmy hedgehog (Atelerix albiventris) was evaluated for severe respiratory distress. Physical examination findings included marked dyspnoea, cyanosis and tachypnoea. Radiographic findings included an enlarged heart and pulmonary oedema, and dilated cardiomyopathy was confirmed via echocardiogram. The patient was treated for congestive heart failure because of dilated cardiomyopathy with furosemide, enalapril, pimobendan and l-carnitine. Within 24 hours of treatment, the pulmonary oedema and cyanosis had resolved. Following discharge, clinical improvement was noted by the owner and echocardiogram confirmed improved fractional shortening. Cardiomyopathy has been reported at post-mortem examination in hedgehogs, but there are no reports of ante-mortem diagnosis and treatment. Performing baseline cardiac assessment in hedgehogs is recommended, and treatment with l-carnitine and pimobendan may improve outcome, as carnitine deficiency is a possible cause of cardiomyopathy in hedgehogs. Successful emergency treatment of congestive heart failure in the hedgehog of this report may be effective for other hedgehogs presented with similar clinical signs.

A 4-year-old crossbred Quarterhorse mare was submitted to the Clemson Veterinary Diagnostic Center for necropsy examination with a chronic history of inappetence, weight loss and lethargy. Prior to death the horse had developed mild diarrhoea and began showing evidence of colic. Necropsy examination revealed a markedly enlarged heart due predominantly to marked dilation of the right atrium, tortuous congested mesenteric blood vessels, marked ascites, pleural effusion and pulmonary oedema. Further examination of the heart showed the endocardium of the left side of the heart, including the mitral valve leaflets, to be diffusely thickened. Microscopically, the endocardial thickening was due to deposition of fibrous connective tissue and elastin fibres. These findings are consistent with a diagnosis of endocardial fibroelastosis.

Background The value of family history (FH) is well established, but its sensitivity to detect familial dilated cardiomyopathy (FDC) has been infrequently examined. Methods A genetic ancillary study was created as a component of the HF-ACTION trial, a multicenter, prospective, randomized clinical trial of exercise in patients with heart failure and an ejection fraction

The atrocious food habit and modern life style stimulate the prevalence of stenosis. Stenosis of pulmonary artery branches is an anomaly characterized by narrowed segments of one or more of the main or peripheral branches of the pulmonary artery. This narrowing may force the heart to pump harder, leading to enlarged heart and high blood pressure in the right ventricle and it results in heart failure and lung related disease like chronic obstructive pulmonary disease. To analyze deviations in pressure and velocity in blood flow, the artificial 3D model of different stages of stenotic condition in pulmonary artery is to be created using ANSYS 15 (Autodesk Inventor Software). Through this analysis certain range of pressure and velocity is obtained. This value helps in understanding the treatments suitable for desired stenosis condition.

The clinical presentation, autopsy findings and toxicology results in an acute fatality involving N-ethylpentylone, a new cathinone derivative, are described. Law enforcement transported a male who was agitated and exhibiting unusual behavior to a local hospital. Upon arrival at the hospital, his body temperature was 105.5 degrees Fahrenheit and his blood pH was 6.7. Clinical laboratory analysis revealed elevated troponins, rhabdomyolysis, hypoglycemia, hepatic and renal injury, respiratory failure and disseminated intravascular coagulation. He was intubated and admitted to the intensive care unit, treated with cooling blankets, bicarbonate and intravenous fluids. Despite medical treatment, he went into cardiac arrest and was pronounced dead ~36 h after admission. Autopsy findings identified some abrasions on his arms and legs, a bloody nose and a mildly enlarged heart. Antemortem blood was analyzed by gas chromatography coupled with a mass spectrometer which identified N-ethylpentylone. Based on clinical presentation, autopsy findings and toxicology results, the medical examiner concluded the cause of death was intoxication by N-ethylpentylone and the manner of death was accident.

Sudden death is common in Africans especially in males in their middle ages. With increasing evidence in reduction of life expectancy among the populace due to several confounding factors there is need to review some of the causes of sudden unexpected death. The study came from the observation of the authors on autopsy requests and reports in Calabar. Two middle aged security officers attached to different private homes were found dead on their duty posts on different days. Autopsy reports on them were similar revealing enlarged heart with evidence of myocardial infarction. Other findings include fatty change, pulmonary oedema and contracted kidneys. Hypertensive heart disease is a common disease condition with resultant high morbidity and mortality if not diagnosed early and well managed.

Infective endocarditis is defi ned as an infection of the endocardial surface of the heart. Its intracardiac effects include severe valvular insuffi ciency, which may lead to intractable congestive heart failure and myocardialabscesses. This disease still carries a poor prognosis and a high mortality.A severe case of infective endocarditis with its complications is presented. A man with aortic prosthetic valve due to earlier aortic stenosis and corrected aortal coarctation and implanted pacemaker presentedwith prolonged unexplained fever, malaise, sweating, weight loss (15 kg/4 months) and lumbar pain. He was treated with broad-spectrum antibiotics prior IE diagnosis was considered. Echocardiogram showedaortic vegetations and possible periaortal abscess formation. Nonspecifi c infl ammation parameters were high positive. Cultures were constantly negative. His condition had deteriorated suddenly, and he had presentedwith worsening of cutaneous vasculitis, subacute glomerulonephritis and subsequent acute respiratory distress syndrome and septic shock. This patient survived with residual bilateral necrosis of the feet andtoxic peroneal paresis. At the end transthoracic echocardiogram showed enlarged heart chambers, LV mild dilated and concentric hypertrophy with ejection fraction about 40%, degenerative postinfl ammatory mitralvalve changes, mild mitral regurgitation and tricuspid regurgitation, postinfl ammatory aortic root fi brosis and moderate aortic valve stenosis (AVPG max 50,9 mmHg, AVPG mean 24 mmHg) with no pericardial effusion. Initial suspicion of Q fever was defi nitely excluded by serological testing showing nonspecifi c IgM positivity,probably rheumatoid factor related.