Endothelial nitric oxide synthase (eNOS) gene polymorphism (Glu298asp) and nitric oxide (NO) levels in patients with ST-segment elevation myocardial infarction (STEMI).

BACKGROUND: Genetic polymorphism in endothelial Nitric Oxide Synthase (eNOS) are associated with occurrence of multiple cardiovascular diseases (CVDs). METHODS: This study included 300 young ST-segment elevation myocardial infarction (STEMI) patients and 300 healthy controls. STEMI patients were divided into two groups: premature coronary artery disease [CAD] (STEMI<40 years of age) and older STEMI (>40 years of age). Genetic polymorphisms in the eNOS gene (894G/T) was evaluated in both subjects and controls. Plasma levels of nitric oxide (NO) were estimated for both patients as well as controls. RESULTS: Mean age of the study population was 49.7 ± 9.2 years with premature CAD being present in 58 (19.3 %) patients. No significant difference at genotypic (P = 0.589, odds ratio (OR) = 0.9, 95 % CI = 0.6-1.6) and allelic level (P = 0.173, OR = 1.2, 95 % CI = 0.9-1.4) was observed between STEMI patients and healthy controls. Genotype 894 TT had significantly higher frequency in STEMI patients >40 years (P = 0.047, OR: 2.5; 95 % CI = 1.0-6.0). No significant difference at genotypic (P = 0.279) and allelic level (P = 0.493) was observed between premature CAD (STEMI age <40 years) and healthy controls. NO levels (131 ± 59.6 µM vs 118.11 ± 49.96 µM; P = 0.001) was significantly higher in healthy controls as compared to STEMI patients >40 years of age (P= 0.001). CONCLUSION: There was significant association of eNOS gene polymorphism Glu298Asp with STEMI patients > 40 years. However, this association was not observed in premature CAD patients. Lower levels of NO in STEMI patients >40 years suggests its potential role as a marker of CVD.

Association between the Glu298Asp and 4b/4a polymorphisms of endothelial nitric oxide synthase and coronary slow flow in the North Indian population.

RATIONALE: Genetic variants in endothelial nitric oxide synthase gene (NOS3) leading to endothelial dysfunction may be predispose to the coronary slow-flow phenomenon (CSFP). METHODS AND RESULTS: In this study, we examined the relationship between Glu298Asp (894G/T) and 4b/4a polymorphisms of NOS3 and CSFP. A total of 27 patients with CSFP but otherwise normal coronary arteries (mean age 50.4±8.2 years) and 200 controls with a normal coronary angiogram (mean age 53.1±8.6 years) were screened for Glu298Asp and 4b/4a polymorphisms by restriction fragment length polymorphism and PCR, respectively. Nitric oxide levels were determined using Griess' enzymatic method for an association with the polymorphisms. The genotype distribution of the Glu298Asp polymorphism differed significantly between the CSFP patients and controls (P=0.004). The dominant genetic model showed that GT+TT was significantly prevalent in patients in comparison with controls (P=0.014) and the T allele was significantly prevalent in patients (P=0.002). The genetic distribution of 4b/4a differed significantly for the heterozygous genotype ba (P=0.047). The overdominant genetic model re-established that the ba genotype was significantly prevalent in patients (P=0.044). Nitric oxide level was higher in patients than in controls, the values being 144.51±43.25 and 129.64±29.47 µmol/l, respectively (P>0.05). The genotypes of Glu298Asp showed a trend of association with nitric oxide levels, which decreased linearly in the order of GG, GT, and TT (P>0.05). CONCLUSION: The Glu298Asp polymorphism of NOS3 associates with CSFP.

Pericardial-peritoneal window: a novel palliative treatment for malignant and recurrent cardiac tamponade.

Transdiaphragmatic approach to the pericardium through a subxiphoid incision is a safe, rapid, and effective way to obtain drainage of the pericardium fluid in patient of disseminated malignancy with recurrent cardiac tamponade. No drainage tubes are needed; pericardial fluid is absorbed by the peritoneum; there is no need for double lumen tubes for single lung ventilation and the subxiphoid incisions are small and almost painless.

Cytologic aspects of T-cell acute lymphoblastic leukemia presenting as a massive pericardial effusion: a case report.

BACKGROUND: Acute lymphoblastic leukemia (ALL) with a clinical presentation of cardiac tamponade and the presence of blasts in the pericardial fluid is an uncommon event. A cytopathologist needs to adopt a cautious interpretive approach while dealing with a lymphoid-rich pericardial effusion in order to prevent a false negative diagnosis. CASE: A 27-year-old male presented with breathlessness, ascites, bilateral pedal edema and fever. He had mild hepatomegaly. On detailed clinical examination, a diagnosis of anemia with cardiac tamponade was made. Cytology of pericardial fluid revealed a large number of lymphoid cells in a hemorrhagic background that, under low magnification, closely resembled mature lymphocytes. However, a careful examination of May-Grünwald-Giemsa-stained cytologic smears, under an oil immersion objective (x 1,000), showed atypical lymphoid cells having blastoid morphology. Rare lymphoid cells displayed a "hand mirror" appearance. A hematologic workup was carried out to exclude leukemia/lymphoma. Complete blood count revealed pancytopenia with abnormal lymphoid cells. Bone marrow showed replacement by 90% lymphoblasts exhibiting periodic acid-Schiff stain, CD3 and terminal deoxynucleotidyl transferase positivity. A diagnosis of T-cell acute lymphoblastic leukemia (FAB L1) was offered, and the patient was started on a remission and induction regimen. However, he had a rapid downhill course and died of cardiorespiratory arrest. CONCLUSION: Both clinicians and cytopathologists need to be aware of rare instances in which ALL may present with a pericardial effusion as an initial manifestation. The abnormal lymphoid cells found in the pericardial fluid in such situations need to be interpreted cautiously, as their presence is of clinical significance.