Teresa Wagner

The relationship of myocardial bridges to coronary artery dominance in the adult human heart

Myocardial bridging is recognized as an anatomical variation of the human coronary circulation in which an epicardial artery lies in the myocardium for part of its course. Thus, the vessel is ‘bridged’ by myocardium. The anterior interventricular branch of the left coronary artery has been reported as the most common site of myocardial bridges but other locations have been reported. The purpose of this study was to provide more definitive information on the vessels with myocardial bridges, the length and depth of the bridged segment, and the relationship between the presence of bridges and coronary dominance. Two hundred formalin‐fixed human hearts were examined. Myocardial bridges were found in 69 (34.5%) of the hearts with a total of 81 bridges. One bridge was found in 59 of these hearts and multiple bridges were observed in ten (eight with double bridges and two with triple bridges). Bridges were most often found over the anterior interventricular artery (35 hearts). Bridges were also found over the diagonal branch of the left coronary artery (14), over the left marginal branch (five) and over the inferior interventricular branch of the left coronary artery (six). Bridges were also found over the right coronary artery (15 hearts), over the right marginal branch (four) and over the inferior interventricular branch of the right coronary artery (two). The presence of bridges appeared to be related to coronary dominance, especially in the left coronary circulation. Forty‐six (66.6%) of the hearts with bridges were left dominant. Forty‐two of these had bridges over the left coronary circulation and four over the right coronary circulation. Seventeen hearts (24.6%) were right dominant. Eleven of these had bridges over the right coronary circulation and six over the left coronary circulation. The remaining six hearts were co‐dominant with four having bridges over the left coronary circulation and two over the right coronary circulation. The mean length of the bridges was 31 mm and the mean depth was 12 mm. The possible clinical implications of myocardial bridging may vary from protection against atherosclerosis to systolic vessel compression and resultant myocardial ischaemia.

An anatomical classification of the variations of the inferior phrenic vein

The majority of anatomical textbooks of gross anatomy offer very little information concerning the anatomy and distribution of the inferior phrenic vein (IPV). However, in the last decade, an increasing number of reports have arisen, with reference to the endoscopic embolization of esophageal and paraesophageal varices, as well as venous drainage of hepatocellular carcinomas (HCC). The IPV is one of the major sources of collateral venous drainage in portal hypertension and HCC. The aim of this study was to identify the origin and distribution of the IPVs (right and left), both in normal and (selective) pathological cases. We have examined 300 formalin-fixed adult cadavers, without any visible gastrointestinal disease, and 30 cadavers derived from patients with HCC. The right IPV drained into the following: the inferior vena cava (IVC) inferior to the diaphragm in 90%, the right hepatic vein in 8%, and the IVC superior to the diaphragm in 2%. The left IPV drained into the following: the IVC inferior to the diaphragm in 37%, the left suprarenal vein in 25%, the left renal vein in 15%, the left hepatic vein in 14%, and both the IVC and the left adrenal vein in 1% of the specimens. The IPVs possessed four notable tributaries: anterior, esophageal, lateral and medial. The right IPV served as one of the major extrahepatic draining veins for all 30 cases of HCC. These findings could have potential clinical implications in the transcatheter embolization of esophageal and paraesophageal varices, as well as in mobilizing the supradiaphragmatic segment of IVC.

The clinical anatomy of the crista terminalis, pectinate muscles and the teniae sagittalis.

The crista terminalis (CT) is an important anatomic landmark due its close association with the sinoatrial node artery and the origin of the pectinate muscles (PM). However, the gross anatomy of the PM in relation to the CT has not been well described. The aim of our study has been to investigate the location and the morphology of PM in relation to the CT. We examined 300 adult formalin-fixed human hearts. All PM originated from the CT and extended along the wall of the appendage toward the vestibule of the tricuspid valve. It was observed that the PM varied significantly with respect to arrangement and course of its fibers. We were able to classify the course of the PM, including the most prominent PM called the tenia sagittalis (TS), into 6 different patterns with 3 different TS types. In Type A (15%), the TS was absent. Type B (65%) demonstrated a single TS and Type C (20%) was characterized by the presence of multiple TS. Furthermore, the course of the PM was classified into 6 patterns: Type I (40%), the PM was oriented perpendicular to the CT with uniform spacing and lack of crossover (trabeculation); Type II (20%), non-uniform PM was organized in a haphazard, trabecular fashion with numerous crossovers; Type III (15%), the PM had uniform spacing with no trabeculation with fibers oriented parallel to the CT; Type IV (10%), had arborizing PM originating from a common muscular trunk (solitary trunk); Type V (10%), fibers were oriented both perpendicular and parallel to the CT, similar in architecture to Type III, but with more than one common muscular trunk; Type VI (5%), prominent muscular column with velamentous PM with potential implications in cardiac catheterization procedures. The exact morphology of PM and TS may be clinically important in right atrial catheterization procedures, as well as in the development of arrhythmias but further investigations are now necessary to prove this theory.

Mucosa-associated lymphoid tissue lymphoma (MALT) of salivary glands and scleroderma: a case report

The connection between scleroderma and lymphoma is uncommon and its pathogenic relationship is a much debated subject. We describe the case of a patient with mucosa-associated lymphoid tissue lymphoma (MALT) of both parotid glands without clinical signs of Sjögren’s syndrome who simultaneously developed scleroderma. Independently of the pathogenic mechanism of these two diseases, it seems very important to emphasize that scleroderma may be the first manifestation of lymphoma.

Obliteration of cardiomyocyte nuclear architecture in a patient with LMNA gene mutation

OBJECTIVE The aim of our study was to perform an immunohistochemical and ultrastructural analysis of the nuclear architecture of cardiomyocytes from an end-stage DCM patient with a missense point mutation in the exon 3 of the LMNA gene which is predicted to result in a D192G substitution. METHODS We studied endomyocardial biopsy samples taken from the right ventricle by immunostaining using antibodies against the lamins A and C and by electron microscopy. The cardiomyocyte ultrastructure was analysed, with particular attention to the nuclear architecture. RESULTS Thirty percent of cardiomyocyte nuclei from the D192G carrier showed chromatin disorganization and a changed nuclear shape. The most surprising finding was the appearance of sarcoplasmic organelles within the nuclear matrix of well enveloped nuclei. To our knowledge, this intriguing phenomenon was observed for the first time in cardiomyocytes. CONCLUSION The study documents that D192G mutation in LMNA gene may lead to the disruption of the nuclear wall in cardiomyocytes, thus supporting the mechanical hypothesis of dilated cardiomyopathy development in humans, which might be mutation-specific.

Unexpected eosinophilic myocarditis in a young woman with rapidly progressive dilated cardiomyopathy

We present the case of 23-year-old woman with good living conditions, one year history of ventricular arrhythmia and 6 months history of decreased exercise tolerance, who was found to have dilated cardiomyopathy after aborted sudden death. Endomyocardial biopsy did not show specific findings. Within 3 months she developed profound bradycardia requiring pacemaker implantation and refractory heart failure, treated with heart transplantation. Intense eosinophilic myocarditis was found in the explanted heart. Retrospective analysis of the patients blood count revealed mild eosinophilia (eosinophil count: 0.86 x 109/l) on one examination only. Following heart transplantation the patient had persistent eisinophilia (eosinophil count: 0.62 x 109/l). Although there was no proven parasitic infestation, based on positive family history of Enterobius vermicularis infestation she was treated with broad-spectrum antiparasitic agent: albendazole and her eosinophil count returned to normal values. This case shows that active eosinophilic myocarditis may present clinically as progressive dilated cardiomyopathy with severe involvement of conduction system. Massive myocardial tissue eosinophilia occurred in the setting of mild and transient blood eosinophilia. Favourable outcome following antiparasitic treatment suggests a potential parasitic infestation as a cause of the disease.