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    We have in the past 2 decades witnessed hundreds of thousands of runners participating in marathons across the globe. Last year Dennis Kimetto set the world record in the Berlin Marathon at 2:02:58. Kimetto not only beat every body who ran in that marathon but every one else who had ever shown up before any where as he blazed his way to a sub 2 hour 3 minutes record time. His record is still intact. The world has rapidly decided to run longer and at the fastest pace possible. The current mantra is to run many miles at blistering speed in the belief that this will cut down disease and death. Recent data however suggest that this may not be the case; and is actually a partial truth. Running undoubtedly is one of the best methods to significantly reduce mortality, heart disease, hypertension, osteoporosis, diabetes, depression and probably cancer. But the question is how much running is therapeutic or healthy. Phidippides was possibly the first running courier to run 26 miles from a battlefield close to the city of Marathon to Athens to deliver the momentous news of victory against the Persians in 490 BC; but the man collapsed almost immediately after and died. Running too much over decades at race speed is now being considered over dosage; much like intake of excessive medicines resulting in harm to the human body.

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    They reckon the population of Delhi NCR is over 20 million and that two thirds of these are young people. One can safely presume that around half are in their thirties and forties; that is almost 10 million people. Epidemiological data indicates that more than a fourth of these young people suffer from hypertension defined as blood pressure exceeding 140/90 mm Hg. That is a sizable population at risk for heart disease and stroke. There is substantial evidence that treating moderate and severe hypertension significantly lowers death, heart disease and stroke. But when you enter the area of mild hypertension the evidence has been equivocal. Mils hypertension is defined as systolic blood pressure 140 to 159 mmHg and diastolic between 90 to 99 mm Hg.

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    The European Society of Cardiology, unlike the US guidelines that recommend dual anti-platelet therapy (DAPT) consisting of aspirin and a P2Y12 inhibitor such as prasugrel, ticagrelor or clopidogrel be used for at least 12 months subsequent to a percutaneous coronary intervention (PCI) procedure, has reduced DAPT duration to only 6 months for drug eluting stents (DES). One month of DAPT is advised for bare metal stent (BMS) deployment (class I), and less than 6 months in patients with high bleeding risk who receive newer generation DES (class II b). It must be noted that randomized clinical trials (RCT) have not demonstrated benefit from prolonged DAPT. The American College of Cardiology/American Heart Association guidelines advise 12 months of DAPT in patients treated with DES, who are not at high risk of bleeding.

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    Recently a middle-aged man presenting with non ST-segment elevation myocardial infarction (NSTEMI) with significant distal left main disease involving ostia of the left anterior descending (LAD) and left circumflex (LCX) arteries consented for percutaneous coronary intervention (PCI). He underwent successful distal left main stenting with TAP stenting for the LCX lesion, but almost immediately developed a large thrombus in the LAD artery, that was managed with an intra-coronary high dose tirofiban injection. The patient had been pre-loaded both with aspirin and 60 mg of prasugrel before coronary angiography. This case suggested the futility of pre-loading with prasugrel but raised other questions such as the role of upstream glycoprotein IIb/IIIa inhibitors (GPI), particularly in patients with distal left main disease.

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