Biomedical subjects

Erik Mont

Publications and source records attributed to Erik Mont.

4 recordsLinked to original sources

PubMed2006

Sources of error and interpretation of plaque morphology by optical coherence tomography.

This study was performed to assess the strengths and weaknesses of optical coherence tomography (OCT) intravascular imaging in identifying plaque morphology. Seventy-nine postmortem human coronary arterial sections classified as fibrous-cap atheromas, calcific plaques, fibrous plaques, and complicated lesions were studied. OCT was able to identify 45% of fibrous-cap atheromas (kappa=0.27, p<0.01), 68% of fibrocalcific plaques (kappa=0.40, p<0.001), 83% of fibrous plaques (kappa=0.37, p<0.001), and 100% of complicated lesions (all thrombi; kappa=1, p<0.001). Misinterpretation was caused mainly by the low OCT signal penetration, which could not detect lipid pools or calcium behind thick fibrous caps, and by an inability to distinguish calcium deposits from lipid pools or the opposite. Lesions with thick (>150 microm) caps were histologically identified as 25 thick fibrous-cap atheromas, 8 fibrocalcific plaques, and 5 fibrous plaques; all these lesions were relatively "stable." In contrast, lesions with fibrous caps<150 microm were either vulnerable or stable lesions (11 thin-fibrous-cap atheromas and 11 fibrocalcific plaques). In conclusion, although OCT images may give an indication of the overall composition of large homogenous signal-poor regions, such as lipids or calcified areas, they could be unreliable in differentiating areas with heterogenous compositions. OCT may easily recognize relatively stable lesions.

Artifacts↗

PubMed2005

Role of SCN5A Y1102 polymorphism in sudden cardiac death in blacks.

BACKGROUND: The Y1102 polymorphism of the cardiac sodium channel (SCN5A) gene has been found in 13% of black Americans. It has been linked to lethal arrhythmias in black families with ventricular tachycardia. The prevalence of the Y1102 polymorphism in a series of sudden death in blacks is unknown. METHODS AND RESULTS: We investigated the incidence of the Y1102 polymorphism in a series of 289 sudden deaths in blacks by sequencing an amplified segment of DNA that contained the polymorphic site extracted from prospectively sampled frozen splenic tissue. The deaths were classified as noncardiac controls (n=107), cardiac arrhythmias with clear anatomic substrate (n=117), cardiac arrhythmias with no anatomic substrate except mild to moderate cardiac hypertrophy (n=40), and unexplained cardiac arrhythmias (n=25). Cause of death was determined after complete forensic autopsy and postmortem cardiac examination. The overall frequency of the Y1102 polymorphism was 9.0%. The frequency was 5.6% in noncardiac deaths, 4.3% in cardiac deaths with obvious anatomic substrate, 20.0% in arrhythmias with moderate hypertrophy, and 28% in unexplained arrhythmias. Adjusted for age and sex, the relative risk of an unexplained arrhythmic death was 8.4 (95% CI 2.1 to 28.6, P=0.001) with the Y1102 allele compared with noncardiac deaths. The relative risk for cardiac arrhythmias with mild cardiac hypertrophy was 4.9 (95% CI 1.3 to 13.4, P=0.01). CONCLUSIONS: The Y1102 allele is a risk factor in blacks for sudden cardiac death in the absence of obvious morphological findings or mild to moderate cardiomegaly.

Adolescent↗

PubMed2005

Left ventricular noncompaction: a pathological study of 14 cases.

Left ventricular noncompaction (LVNC) has been recently proposed as a specific form of cardiomyopathy. There have been few pathological series describing gross and microscopic findings of this entity, especially in children. We present findings of 14 hearts (13 autopsy and 1 explant) with LVNC (isolated and associated with congenital heart disease), defined by poorly developed left ventricular (LV) papillary muscles and a noncompact inner LV myocardial layer comprising more than 50% of the LV thickness. The mean age at death/explant was 3.6 years (median, 2.5 months); there were 6 boys and 8 girls. The symptoms were sudden unexpected death (10) and heart failure (4). The diagnosis was suspected before death in only 1 of 13 autopsy cases. Right ventricular involvement (> 75% ventricular thickness comprised of noncompacted area with recess adjacent to tricuspid valve) was seen in 6 of 14 hearts. One patient had a sibling with pulmonary stenosis, but there was no other known familial cardiomyopathy. Endocardial fibroelastosis was a characteristic histological feature, as well as anastomosing or polypoid endocardial trabeculations, which resulted in staghorn-shaped, endocardial-lined recesses. There was a high rate of other cardiac anomalies, which often coexisted and were not clearly related to the LVNC, present in 8 cases (nonisolated LVNC): ventricular septal defect (4/14), anomalous venous pulmonary veins (1/14), coronary ostial stenosis (1/14), histiocytoid cardiomyopathy (1/14), polyvalvar dysplasia (2/14), and pulmonary stenosis (2/14). In the 6 isolated LVNC, there were 2 malformed atrioventricular valves (1 mitral and 1 tricuspid), which appeared part of the ventricular maldevelopment. There were no differences in histological or gross patterns of the noncompacted regions between the isolated and nonisolated LVNC. LVNC is frequently associated with other cardiac defects, especially when causing sudden death in infants and children. A clear-cut morphological distinction between "isolated" and "secondary" LVNC was not apparent. The pathologist should be aware of the entity because the diagnosis is often first established at autopsy.

Autopsy↗

PubMedDate not supplied

Thrombotic thrombocytopenic purpura causing rapid unexpected death: value of CD61 immunohistochemical staining in diagnosis.

BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) shares histologic features with disseminated intravascular coagulation (DIC) but is clinically distinct. TTP may result in myocardial hemorrhages and rapid death. We compared rapidly fatal TTP with heart involvement and DIC cases to determine if the differential diagnosis of TTP and DIC could be aided by immunohistochemical techniques. DESIGN: We examined 11 hearts from seven women and four men dying with TTP (aged 34+/-10 years) and 8 hearts from patients dying with DIC (five women, three men, aged 58+/-16 years). The diagnosis of TTP was established on histologic findings and identification of thrombocytopenia with schistocytes on premortem blood smear. Underlying conditions for TTP were recent diarrheal illness (3), autoimmune disease (3), sickle cell disease, HIV infection, cocaine abuse, and none known (2). Underlying conditions for DIC were disseminated carcinoma (4), multiorgan failure after open-heart surgery (2), pancreatitis (1), and placental abruption (1). Antibodies against platelet glycoprotein IIIa (CD61) and fibrin II were applied to formalin fixed tissue sections and detected by the avidin biotin techniques, and platelet and fibrin capillary thrombi were quantitated. RESULTS: Gross myocardial hemorrhages were present in 7/11 cases of TTP and 0 cases of DIC (P<.001). Capillary thrombi were present in all cases by routine histologic techniques but were often difficult to discern. Platelet thrombi were strongly highlighted by stains for CD61 and seen at a density of 8.0+/-3.1/mm(2) in TTP versus 0.5+/-0.4/mm(2) in DIC (P=.0001). In TTP, there were 12.1+/-5.9/mm(2) fibrin capillary thrombi and 4.8+/-5.8/mm(2) in DIC (P=.05). CONCLUSION: In the myocardium, rapidly fatal TTP is characterized by the diffuse presence of intracapillary platelet-rich thrombi, in contrast to DIC, which is characterized by predominantly fibrin thrombi. Immunohistochemical staining for CD61 and fibrin II is helpful in diagnosing TTP and distinguishing it from DIC.

Adult↗