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Pediatric hypertension is an emerging problem in the developed and developing countries alike. I would like to congratulate the authors of the article titled “evaluation of sustained blood pressure elevation in children” for doing a commendable job of shedding light on this important topic.1 Along the same lines we would like to highlight some important points. First and foremost, the statistical analysis section mentions that the p value is 0.5 which we consider is quite unusual taking into consideration that it is usually set at 0.05 or 0.001 at the discretion of the investigator of the study.1 Yet, if this is the p value considered then the values mentioned in Table 3 and the textual interpretation of the same do not match. In the text, authors have mentioned that of all the variables considered only age and weight showed significant association to hypertension. Interpretation of Table 3 shows that the variables socioeconomic status (p = 0.408) and weight (p = 0.01) are significantly associated with hypertension and other variables of height (p = 0.83), sex (p = 0.83) and age (p = 0.74 for boys and p = 0.56 for girls) are not significantly associated with hypertension. This would definitely reflect on the discussion. Secondly, as mentioned by authors most of the cases of hypertension detected belonged to age group 13–15 years. This is the age when pubertal growth starts occurring and this might have influenced the changes in the blood pressure. Such a change has been attributed to the increase in gonadal hormones. Increased hormone secretion during puberty might interfere with known pressor systems as has been mentioned in the literature. This also can be the reason for the gender differences seen in this study as the pubertal changes in males lead to more profound change in BP levels compared to females.2,3 The gender difference in prevalence of hypertension in pubertal age has been well documented. Boys were 10% more likely than girls to develop high SBP as adults.2 High SBP has been reported to be more prevalent among boys than girls in several cross-sectional studies. This suggests that sex steroids may have an important impact on blood pressure levels.4 This factor warrants consideration when we consider such age groups for study. This implies that such adolescents are at higher risk of hypertension as adults. These adolescents can take appropriate precautions so as to prevent complications in terms of its severity and time of onset in the future.

The current study is a prospective, randomized controlled study with two parallel treatment groups done to assess the tolerability and efficacy of a combination of atorvastatin (10 mg) and extended release nicotinic acid (1G) in comparison to atorvastatin (20 mg) alone in modulating the lipid profile in patients of Ischemic Heart Disease in our population.Patients were randomly allocated into two equal groups (n = 216) as per selection criteria. Group A received Atorvastatin 20 mg while Group B received combination of Atorvastatin -10 mg and extended release nicotinic acid (1G), both once daily at bed time, for a period of 24 weeks. Final end-of-study assessment and evaluation of tolerability and efficacy was done after 24 weeks. Comparison between the groups was performed with paired t-test. A p value0.05 was considered to be statistically significant. There was significant reduction in cholesterol, LDLtriglycerides in both the groups. Mean values of cholesterol and LDL were comparable in both groups where as there was increased reduction of triglycerides in Group B. Mean value of HDL cholesterol significantly increased only in group B thus the total cholesterol: HDL ratio was decreased more favorably. SGPT level was not significantly altered in either of the groups.In the Indian perspective, where HDL is low and the LDL values are not very high, a combination of low dose atorvastatin with nicotinic acid may influence the lipid profile more favorably and reduce the cholesterol/HDL ratio in comparison to atorvastatin alone and is also fairly well tolerated.

Platelet aggregation is a key factor behind coronary artery disease. Various complications after an attack of acute coronary syndrome are often related to the platelet hyperactivity in the early hours following the event. There is a growing concern regarding aspirinclopidogrel resistance, which has put the time-tested therapies under scrutiny. Time has come to address the issue of platelet hyperactivity in the early hourswhether to individualize therapy and drug doses in different patients.We prospectively enrolled 41 patients with a diagnosis of acute myocardial infarction (AMI) between July 2009 and July 2010 admitted to the cardiology ward and ICCU of Medical College, Kolkata, after fulfillment of inclusionexclusion criteria. The study was reviewed and approved by the Institutional Ethical Committee. Platelet Aggregation (PA) with 10 microM epinephrine, 2 microg/ml collagen and 10 microM ADP was performed with light transmittance aggregometry in all patients according to the standard protocol. Tests were done within 3 hours of sampling with platelet-rich plasma (PRP) by the turbidometric method in a 2-channel aggregometer (Chrono-Log 490 Model, Chrono-Log Corp, Havertown, Pa). Aspirinclopidogrel resistance were defined as per ACC/AHA guidelines. Platelet aggregation studies were done at presentation (zero hour) and 48 hours after instituting dual antiplatelet therapy in standard doses.Patients with first attack of AMI showed a high mean platelet aggregation at 0 hours of 77.4% +/- 18.8% with ADP, 77.5% +/- 26% with Epinephrine73.5% +/- 24.9% with Collagen. With all three agonists, the initial hyperactivity of platelets at 0 hours was significantly higher among diabeticsobese. Though reduced, significant platelet hyperactivity remained at 48 hours after initiating standard antiplatelet therapy; 50.3% +/- 14.3% with ADP, 56.5% +/- 21.6% with epinephrine38.4% +/- 22% with collagen.In the early hours after AMI there is a fairly high degree of platelet aggregation. Even after 48 hours of standard antiplatelet therapy the platelet aggregation though reduced, still remains significantly high. Since recurrent ischemic episodes frequently occur in this vulnerable period, time has come to assess platelet aggregation status in high risk groups, if not in all patients of acute coronary syndrome during this period so that therapy may be individualized. Further researches are required in this area.

Lung malignancy extending into left atrium is seen very infrequently. We had a patient with a fast growing symptomatic lung mass and electrocardiogram showing persistent coving ST elevation without any biomarker change. Transthoracic echocardiography showed a large left atrial mass which was fixed to the free walls and extended into the appendage. There was also a large lung mass that was compressing the heart from its lateral aspect. CT-scan of chest corroborated the lung massCT-guided FNAC showed small cell carcinoma.

Recurrent ischemic events continue to occur despite combination anti-platelet therapy. Currently aspirin, clopidogrel and dual resistance are increasingly recognized entities. The relationship of such resistance to recurrent ischemic events is largely unknown. In this study, we tried to gain an insight into the role of antiplatelet drug resistance with recurrent Acute Coronary Syndrome (ACS).The antiplatelet effect of aspirin and clopidogrel was studied in 40 recurrent ACS patients and 170 patients with first episode of ACS, afteror = 7 days of dual antiplatelet therapy. Platelet aggregation study was done with optical aggregometer. Resistance to aspirin and clopidogrel was defined asor = 50% aggregation with collagen and ADP respectively.Aspirin, clopidogrel and dual drug resistance were encountered respectively in 35%, 72.5% and 32.5% patients with recurrent ACS. The corresponding figures for the patients with first episode of ACS were 25.3%, 42.3% and 18.8% respectively. P values for the comparisons were 0.237 for aspirin, 0.0007 for clopidogrel and 0.084 for dual drugs. Patients with recurrent ACS were relatively younger and had a higher prevalence of conventional risk factors like hypertension, diabetes and elevated LDL.Antiplatelet drug resistance is likely to play an important role in recurrent ACS alongside other conventional risk factors. Further research is required in this field to have a definitive conclusion.

Platelets play an important role in the pathogenesis of Acute Coronary Syndrome (ACS). Most of the complications of ACS occur during the initial hours of presentation. We tried to gain an insight into the platelet function during the initial phase of ACS in patients on dual antiplatelet therapy.Platelet aggregation study was performed by light transmittance aggregometry in 64 ACS patients 48 hour and 7 days after initiation of dual antiplatelet therapy with aspirin and clopidogrel.Epinephrine, ADP and collagen induced platelet aggregation was significantly higher at 48 hours, following initiation of dual antiplatelet therapy, in comparison to the profile observed on the 7th day. Diabetics demonstrated a significantly higher aggregation at both the time points and aggregation was also somewhat higher in smokers though it did not reach statistical significance.This study conceptualizes the hypothetical role of alpha-2 adrenoreceptor blockers during the early hours following ACS and also warrants further investigations exploring the optimum loading dose of antiplatelet agents, especially clopidogrel in patients with ACS.

Antiplatelet therapy is a cornerstone in the management of the atherosclerotic vascular disease. Aspirin and clopidogrel are the two most commonly used antiplatelet drugs in its management. Recently, there has been a concern about the development of resistance to one or both antiplatelet agents with potentially devastating consequences. In this study we tried to assess the in vitro resistance to antiplatelet agents in patients presenting with acute coronary syndrome (ACS).144 patients presenting with ACS, who were not on any antiplatelet therapy prior to hospital admission were evaluated in this study. Baseline clinical data was obtained before giving the oral loading dose of aspirin and clopidogrel. Patients received a loading dose of 325 mg of aspirin and 300 mg of clopidogrel followed by a daily dose of 150 mg. of aspirin and 75 mg.of clopidogrel. After 7 days of dual antiplatelet therapy, platelet aggregation pattern was analyzed using optical aggregometer (chrono-log). Response to aspirin and clopidogrel was assessed by interaction with collagen (2microg/ml) and Adenosine diphosphate (ADP) (10micro/ml) respectively. The results were analyzed. Response to doubling the dose of antiplatelet agents was also observed in 6 aspirin resistant patients, 12 clopidogrel resistant patients and in 6 patients resistant to the effect of dual antiplatelet agents.There were 22 patients (15.27%) who showed poor response to aspirin, 28 patients (19.44%) to clopidogrel (primary non-responder) and 18 patients (12.5%) showed a primary non-responsiveness to both the antiplatelet agents in the usual doses. After dose doubling, all 6 aspirin resistant patients showed adequate response but 4 out of 12 clopidogrel resistant patients showed inadequate response.This pilot study brings out a disquieting picture of 12.5% patients suffering from ACS showing resistance to the antiplatelet effects of both aspirin and clopidogrel in the conventional dose. A long-term prospective randomized controlled trial is required to give an insight into this problem and its clinical consequences.