Background: Increased incidence of cardiac involvement and pulmonary hypertension (PH) has been reported in patients with chronic myeloproliferative disorders (CMPD). Most studies are small and retrospective except one where majority of the patient had essential thrombocytosis (ET). Method: We conducted a study to assess the incidence of PH in patients with CMPD. Patients were excluded if they had secondary cause of PH. Diagnosis of PH was established if right ventricular systolic pressure (RVSP) by transthoracic echocardiography (TTE) and Doppler study was ≥ 35 mmHg. 27 patients with diagnosis of CMPD established by standard criterion were included in the study. 9 patients had ET, 14 had polycythemia vera (PV) and 3 had chronic myeloid leukemia (CML). Results: Diagnosis of PH was established in 14/27 patients. 2 patients were excluded form analysis because of poor ejection fraction on TTE, 1 with PV and 1 with CML, giving final diagnosis of PH in 12/25 (48%) patients. 9 patients were males and 16 were females. Mean age at diagnosis in the entire cohort was 56.2 years and that with and without PH was 54.5 vs. 57.7 years respectively. Mean duration of follow up was 8.7 years and that with and without PH was 7.8 vs. 9.9 years respectively. 7/9 ET, 5/14 PV AND 0/2 CML patients had PH, mostly of mild to moderate severity. All patients were asymptomatic at the time of their last visit within last 2 months. The results are depicted in the table 1. There was no relation of PH to duration of disease, platelet count and hematocrit at diagnosis or during follow up period for the entire group or specific diagnosis of ET or PV. Because of erratic and variable duration of aspirin use by individual patients, we could not determine its significance. Discussion: The results of our study are similar to the study reported by Garypidou et al with regard to ET. However they had only 2 patients with PV and both of them had no evidence of PH. In our study 5/14 PV (36%) patients had PH, indicating PV patients also have significant risk of having PH. Pathogenesis of PH can be reliably related to CMPD because: Cases of secondary PH were excluded TTE excluded cardiac causes of PH Incidence of primary PH is very low (0.2cases/100,000) and usually occurs in 3rd or 4th decade. Moreover autopsy studies have demonstrated the presence of atypical megakaryocytes and thrombotic material in the lung capillaries of pulmonary hypertension patients and CMPD. Increased level of thrombopoietin also has been demonstrated in pulmonary artery of patients with PH. Thus platelets are implicated in pathogenesis of PH in patients with CMPD. Since PH seems to be common in patients with CMPD, more studies are needed to study the long-term impact of PH on survival in these patients. Impact of therapy including platelet lowering agents and ASA on development and progression of PH also needs to be studied. Table 1 CMPD Total No (%) MeanAge at Dx(yrs) Duration of Ds(yrs) Mean Plt at Dx(k/muL) Mean Plt at fu(k/muL) Mean Hct at Dx(%) Mean Hct at fu(%) Dx-diagnosis, Ds-disease, yrs-years, Plt-platelet, fu-follow up, Hct-hematocrit, PH-pulmonary hypertension, +-present, − absent ET PH + 7/9(77.8) 56.3 7.2 877.7 488.6 41.1 36.7 ET PH − 2/9(22.2) 65.0 8.0 698.0 492.0 45.3 40.0 PV PH + 5/14(35.7) 52.0 10 528.8 320.4 53.9 43.2 PV PH − 9/14(64.3) 58.7 10.6 511.9 316.8 58.9 41.9 CML PH − 2/2 46.5 4.0 620.5 387.5 36.9 36.2

BackgroundElevation of C-reactive protein (CRP) is a marker of adverse outcomes in acute coronary syndromes (ACS). Its role has not been evaluated in patients with stable coronary artery disease (CAD) and in those who are undergoing stress test for risk stratification. We hypothesized that patients with a positive stress test are more likely to have higher CRP levels than patients with a negative stress test.MethodsPatients who underwent stress test for CAD evaluation or risk stratification had a CRP level drawn prior to the stress test after an informed consent was obtained. The lower limit of CRP is 0.5 at our institution and the test is of intermediate sensitivity. The stress test was performed as per clinical indication and at the attending cardiologist's discretion. Patients underwent either exercise or pharmacological stress nuclear SPECT test.ResultsTotal of 93 patients' results were available for analysis. CRP was positive in 7 out of 0 patients with positive stress test. CRP values being 0.6, 0.7, 0.9, 0.9, 1.6, 2.8, and 3.0 with a mean of 1.5. The patient with highest CRP value died of acute coronary event ten days after the stress test. Only 2 patients who had a positive stress test had negative CRP levels. CRP levels were positive in 7 out of 84 patients who had a negative stress test. The CRP values were 0.6, 0.6, 0.6, 0.6, 0.6, 0.7, and1.2 with a mean of 0.7. Two patients with positive CRP levels in the negative stress test group (including the patient with level of 1.2) had an episode of angina pectoris one week prior to the test. The sensitivity for the test was 77.8% and the specificity was is 91.4% to predict a positive stress test.ConclusionsCRP is a valuable prognostic marker even in patients with stable CAD and in those undergoing risk stratification and can be used as an additional marker in predicting adverse outcomes in patients with stable coronary artery disease. It is complementary to nuclear stress test and can help in identifying high-risk patients who would benefit from aggressive interventions in their management. In patients who had a negative stress test and positive CRP values the values of CRP are low.

Objective: To study the prevalence of Activated Protein C (APC) resistance due to Factor V Leiden (FV Leiden) mutation among the first generation immigrants from India and Pakistan with venous thromboembolism (VTE). Introduction: APC resistance due to the substitution of Arginine 506 by Glutamine in coagulation Factor V is caused by G1691A mutation in exon 10 of Factor V gene. This is the commonest cause of inherited thrombophilia in Caucasians, but the frequency of this mutation is low in non-Caucasians. Among subjects in the Physician Health Study, the frequency of FV Leiden was found to be 5.27% in Caucasian Americans vs. 0.45% in Asian Americans. Another study found no mutation in 191 Asian Americans tested. In non-Caucasians with VTE, it is generally considered not cost effective to screen for this mutation. However Asians are a heterogeneous group and the Leiden gene frequency varies among different ethnic populations. While the frequency of FV Leiden gene has been documented to be low in China, Korea, Japan, Thailand, Indonesia etc, the frequency in India and Pakistan is not well studied. Two studies found a carrier frequency of 2% (Rees et al) and 4.2 % (Gou et al) among the general population from India and Pakistan. This is similar to the frequency found in Middle Eastern and European population. We did not come across any study of FV Leiden gene frequency in patients with VTE from India and Pakistan. Patients and Methods: A retrospective chart review of patients of Indian or Pakistani origin seen at Coney Island Hospital, from July 1996 to June 2003, who had a work up for inherited thrombophilia after an episode of VTE. During the chart review age, sex, first or recurrent episode and any predisposing factors such as immobilization, malignancy, hormonal therapy, surgery, pregnancy, and the presence of SLE or MPD were noted. Thrombophilia work up included functional assays for Protein C, S and Antithrombin III, Lupus anticoagulant, ACA and Homocysteine levels. APC resistance was measured by a clotting assay using Factor V depleted plasma and all patients who were borderline or resistant were tested for the presence of FV Leiden mutation by PCR. Results: A total of 18 patients were studied. All had an episode of VTE documented by a Doppler ultrasonography or a Ventilation Perfusion lung scan or a CT angiogram. 3 out of 18 patients (16.6%) had APC resistance. All the three patients were confirmed to be heterozygous for FV Leiden mutation. Two were male and one was a female with a median age of 36 yrs (27, 36 and 57 yrs). The female patient had a recurrent episode, first one occurred during pregnancy, but the second episode had no precipitating events. One male patient had trauma to the leg and was immobilized at the time of the VTE, another male patient was a cab driver by occupation. None of the patients had any other concurrent inherited thrombophilic state. Conclusions: The prevalence of the FV Leiden mutation is significantly high among South Asians with VTE in our study. If the findings are confirmed by a larger study, screening for this mutation for thrombophilia would be relevant in patients of South Asian origin and screening recommendations for family members would be identical to Caucasian population. The high prevalance as in Caucasians suggests a founder effect and possible spread of the mutation by the migration of Neolithic farmers from the Middle East towards Europe and India, ten thousand years ago. This has been confirmed by haplotype analysis.

subjects are in agreement with animal studies that indicate chronic exercise decreases the expression of VCAM in aorta tissues and suggest that a decreased VCAM expression due to regular EX can be a mechanism for the protection of AS by EX.