Today is World AIDS Day

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What is PrEP?

PrEP is short for Pre Exposure Prophylaxis and may be part of comprehensive HIV prevention services in which HIV-negative people who are at high risk, take antiretroviral medication daily to try to lower their chances of becoming infected with HIV if they are exposed to it.

To date, PrEP has been shown to be effective in men who have sex with men (MSM) and heterosexual men and women.

In November 2010, the NIH announced the results of the iPrEx clinical trial, a large, multi-country research study examining PrEP. The study found that daily oral use of tenofovir plus emtricitabine (TDF/FTC single tablet) provided an average of 44% additional protection to men who have sex with men (MSM) who also received a comprehensive package of prevention services that included monthly HIV testing, condom provision, and management of other sexually transmitted infections.

In July 2011, a new CDC study called the TDF2 study, along with a separate trial by the University of Washington, provided evidence that a daily oral dose of antiretroviral drugs used to treat HIV infection can reduce HIV acquisition among uninfected individuals exposed to the virus through heterosexual sex.

CDC has developed interim guidance for physicians electing to provide PrEP for HIV prevention among MSM. Because pregnant and breastfeeding women were excluded from participation in PrEP trials, further evaluation of available data will be needed before any recommendations can be made regarding the use of PrEP for women during conception, pregnancy, or breastfeeding.

Oral pre-exposure HIV prophylaxis may be an effective therapy to decrease HIV transmission in HIV discordant couples who choose to conceive naturally.

Proceedings of 26th Annual CSI Meet day 2

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Dr Rakesh Yadav on what’s new in pace maker functions

  • Functions of pace makers are to sense properly, pace properly, pace with minimum output and to manage tachy- arrhythmia.
  • New functions are to avoid unnecessary pacing and to pace with minimum output
  • RV pacing is LBBB pattern. De-synchrony is harmful to LV in long term. Therefore pace maker should only pace when required.
  • AAI R, DDD R, DDI R, VVI R and hysteresis are the best answers.
  • Switches from AAIR to DDDR mode automatically.
  • New advances in pace maker: Automatic adjust AV interval.
  • Diarrhea and low K the thresh hold will rise. New machines are automatic thresh hold management
  • New pace makers diagnose and treat atrial arrhythmias. AF suppression pacing.
  • Automatic from bipolar to unipolar mode
  • Remote monitoring and security alerts.
  • RV apex to RVOT or mid septum pacing is better.
  • Should all patients have bi ventricular pacing. The studies are on.

Dr Vivek Chaturvedi on SCA

  • ICD can prevent SCD in young. 10% of all SCD are in normal hearts (normal ECHO). It is important to screen as 25-40% have re attacks in the next 2 years.
  • Commotio Cordis: VF due to blunt non-penetrating trauma, seen in young adults. Cork ball.
  • Long QT syndrome means QTC > 0.44 in men and > 0.46 in women.  QTc on exercise fails to shorten or increase by > 30 ms. Beta blockers of choice. ICD avoided
  • CPVT: stress and exertion are triggers. Beta blockers are effective. Patients present with exertion syncope, palpitation or epilepsy
  • Brugada syndrome: control fever
  • Early repolarisation syndrome: present in 5% population, is not considered normal, 15-70% of idiopathic VF cases have it and quinidine is effective

Dr Balbir Singh on CRT in class I and II heart failure

  • CRT D or CRT or ICD.  CRT triad: Low EF, broad QRS and symptomatic
  • In class III and class IV patients its use is beyond any doubt. In 2002 MIRACLE trial showed 40 % reduction in mortality. In 2004 Companion trials showed similar results. CARE- HF trials also showed 40% reduction in mortality.
  • Beta blockers reduces mortality by 35%, aldosterone antagonism by 22%, CRT by 35%
  • NYHA I and Ii patients are younger, active and with better quality of life. The trials in favor of them are 2004 MIRACLE, 2009 REVERSE and 2009 MADIT CRT.
  • REVERSE trial:  QRS > 120 EF < 40 LVEDD > 55. Optimal medical drugs. Class I or II.  CRT better in terms of less first to hospitalization rate and reverses LV remodeling less hospital admissions. Same results were seen with MEDIT CRT and RAFT trial.
  • Conclusions: EF < 35% and QRS > 120 needs CRT in class III and class IV and EF < 35% and QRS > 150 needs CRT in class II heart failure.

Dr T S Kler on AF treatment management

  • Vernakalant new drug for AF conversion. Yet to be marketed in India.
  • Control of ventricular rate is most important in acute AF.  Rate control should be associated with anti coagulation.
  • Oral anti coagulation is under treated in over 50% of cases with acute AF.

Dr Savitri Srivastava on catheter interventions in Congenital Heart Disease

  • PDA stenting in infants and neonates to avoid BT shunt (more morbidity) for duct dependent lesions. Even can be used after the duct is closed
  • Pulmonary atresia and intact IVS: Perforation of RVOT with RF ablation and stenting of RVOT
  • Coarctation aorta: Stent for children age > 4 and weight > 18 Kg. Not to be done in severe coarctation and long segment coarctation.
  • Balloon dilation of discrete sub aortic stenosis: after age 13, AV to membrane distance > 9 mm.
  •  Per cutaneous PV implant in RVOT conduit stenosis and severe PR.
  • Device closure of RSOV (rupture of sinus of valsalva): RSOV from NCC/RCC > 5 mm away from ostia.
  • AP window with device: 10% suitable.
  • Peri-membranous VSD closure with devices.  Complications is 11.5%
  • Fontan completion by catheter intervention.
  • Hybrid procedures: interventions and surgery together, hybrid OR’s
  • Fetal interventions, severe RV or LVOT obstruction. PFO closure

Dr Sanjay Tyagi on Resistant Hypertension

  • 10% have resistant Hypertension, Non adherence is not included in the diagnosis
  • Kidney plays a critical role.
  • Failure of 3 drugs to control Bp < 140/90
  • OSA, Obesity, NSAIDS, Cox 2, decongestive drugs, diet pills, steroids, anabolic steroids, ESA, cyclosporins are important causes.
  • Primary alodsteronism, uncommonly diagnosed, presents with hypo kalemia. K < 3 and  plasma aldosterone/renin ratio of  > 555 SI units
  • If there is volume expansion give diuretics, or increase its dose or change the diuretic, HCTZ to chlorthalidone
  • Low GFR add Loop diuretics
  • Another drug is cilinidipine, causes no edema, available, reduces  sympathy activity
  • Add 4th drug, which can be spiranalactone, eplerenone ,  alpha bb, Methyl dopa or Clonidine.
  • In OSA give eplerenone as has no sexual dysfunction
  • 2011 atrasentan, darusentan are new additions in the treatment
  • Interventions: stenting of renal artery stenosis (atherosclerotic), fibro myscular dysplasia only balloon dilatation
  • Aorto arteritis: balloon angioplasty
  • Child heart failure with HT 80-90% RAS
  • Cutting balloons for RAS, cutting of intima,
  • Coarctation of aorta: do balloon dilation and use self expandable stents or balloon expandable  stents, avoid in children
  • Renal de-nervation is the latest treatment strategy
  • Carotid baro-receptors stimulation

Dr D S Gambhir on Lipid Management

  • Beyond reduction of LDL
  • 16.7 million deaths in 2002 in the world. 14% due to CAD, 33% stroke
  • Low HDL (80%) more common than high LDL (31%) in south Asians: INTERHEART study.
  • Framingham heart study: Low HDL with high mortality. HDL < 35has 2-4 high times risk of cardiac risk.
  • Maximum risk high LDL and low HDL-C.
  • PROCAM: Low HDL is an independent risk factor for CAD.
  • HDL smallest particle of lipoproteins, Apo A1: 70% of HDL, Apo AII: 20% of HDL.
  • Statins: desired goal not achieved in 43%. Non HDL goal nor achieved in 73%
  • 30% red in risk by statins
  • New approach is to lower LDL, raise HDL and lower T levels
  •  Current guideline is to lower LDL to < 70 and non LDL to < 100
  •  HDL can be reduced by reducing trans fat, increasing activity, reducing refined carbohydrates, stop smoking and taking moderate alcohol
  •  Niacin study AIM-HIGH stopped early
  •  Torcetrapib, anacetrapib, dalcetrapib can increase HDL by blocking CETP
  • HPS-2 AIM HIGH are two recent trials to read
  • Statins can increase uric acid and new onset blood sugar
  • Muscle pain: change to rosuvastatin, it may help, more potent, extra hepatic side effects are lower.

Dr K K Talwar

  • Advanced heart failure is defined  as class II or IV heart failure despite ACE inhibitors, diuretics, digoxin and n and beta blockers. 30-50% mortality at one year. PWP > 16 high mortality
  • Reversible factors: Heavy alcohol, anemia, pulmonary embolism, thyroid disorders, CKD, rheumatic activity, DCM, IE, hibernating myocardium due to CAD
  • 4 sub groups: Warm and dry/ Warm and wet/ Cold and dry/ Cold and wet [Stevenson L W J H fail 2005;7:323-331] based on congestion vs low perfusion.
  • Max mortality wet and cold and least mortality dry and warm. Next best is dry and cold.
  • Warm and dry: Give ACE inhibitors, beta blockers, aldactone (maximum tolerable doses)
  • Warm and wet: Start with diuretics (infusion or bolus), may add metolazone, nitroglycerine,  nesiritide. Do not use inotropes as may be harmful.
  • Cold and wet: do not respond to diuretics, large doses or infusion may be needed, withdraw ACE inhibitors and beta blockers, if high SVR add  nitroprusside or metolazme. Add ACE inhibitors and beta blockers later. Is the largest group.
  • Cold and dry:  smallest group, no inotropes required; gradually add beta blockers, ace inhibitors. No inotropes unless low CO is the concern
  •  Cardiorenal syndrome: seen I n 25% situations, 30% CHF have CKD, use nitrates,stop nephro toxic drugs. Discontinue ACE inhibitors
  • Rule out tachycardia induced CMP

Dr KK Seth on Sub Clinical Atherosclerosis

  • CAD is chronic immune inflammatory disease, remains silent for 7-10 years, may present with plaque rupture
  • Max heart attack in < 70% lesions. TMT may miss these lesions. Angiography may miss these lesions
  • INTERHEART: 9 modifiable risk factors responsible for 90% cases ( smoking, fruits/exercise/alcohol/obesity/hypertension/diabetes/lipids
  • Framingham risk factor score < 10%, 10-20% or > 20%. Now a days one consider low risk as < 5% and 6-20 % as intermediate risk
  • 60-70% events occur in low or intermediate group
  • Zero calcium score  does not rule out CAD
  • AHA consider ACC and CIMT as Aha as class Imia indication, Men > 50 women > 60, India 10 years younger.
  • Do not screen low risk or high risk patients
  • One can have CCS zero and abnormal CIMT; or abnormal CCS and normal CIMT,
  • CCS stronger predictor of CV events and CIMT stronger predictor of stroke
  • Take home message do CIMT first, if > 1 mm or plaque present no further screening required. If CIMT normal then go for CCS.


Annual CSI Delhi Proceedings

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Take Home Messages

1.            Col C P Roy: Stains are safe. The concern about them causing diabetes is of no concern.

2.            Dr Rakesh Yadav: Venous grafts will lose 10% in the first month, another 10% in the firth year and then 2% every year. Bare stents are good enough for graft stenosis.

3.            Dr Sanjiv Sharma: For coronaries angiogram: look for anatomy (origin, course, termination); luminal abnormality; lesion and consequences on LV.

4.            Dr Sanjiv Sharma: all views are not required in coronary angiogram. LA caudal view gives maximum radiation.

5.            Dr Sanjiv Sharma: Never use le than 30 ml contrast in LV angiogram

6.            Dr R Juneja: Lead 2 is the best lead to study electro physiology

7.            Dr R Juneja: Left axis deviation with RBBB has to be ventricular tachycardia

8.            Dr R Juneja: MI with RVOT tachycardia is not due to MI

9.            Dr R Juneja: Do not send cases with bradycardia for EP studies.

10.          Dr S S Kothari: BP of 130 mm Hg rues out constrictive Pericarditis is not true

11.          Dr S S Kothari: BP of > 15 mm Hg systolic rules out AS is not true

12.          Dr S S Kothari: Any amount of gradient in mitral valve is abnormal

13.          Dr Rajnish Sardanna: Dronedarone is a class III antiarrhythmic agent that may be considered for the maintenance of sinus rhythm in patients with atrial fibrillation (AF).

14.          Dr Rajnish Sardanna: Dronedarone has many electrophysiological properties in common with amiodarone, including its antiadrenergic (ie, beta blocking) properties and the ability to inhibit multiple transmembrane potassium, sodium, and calcium currents.

15.          Dr Rajnish Sardanna: In contrast to amiodarone, which has an effective half-life of up to 50 days, dronedarone has a half-life of approximately 24 hours.

16.          Dr Rajnish Sardanna: Because of its hepatic metabolism, there are numerous potential drug interactions with dronedarone. Concomitant use of dronedarone with some medications (eg, ketoconazole, class I antiarrhythmic drugs) is contraindicated, while its use with other medications (eg, digoxin,warfarin, statins) may require dose adjustment.

17.          Dr Rajnish Sardanna: Trials have shown that dronedarone is more effective than placebo but less effective than amiodarone for the maintenance of sinus rhythm in patients with AF. However, dronedarone may be preferred in certain patient populations.

18.          Dr Rajnish Sardanna: Dronedarone (400 mg twice daily) is used for the maintenance of sinus rhythm in patients with paroxysmal or persistent AF or atrial flutter and no evidence of heart failure or left ventricular systolic function who have spontaneously reverted to sinus rhythm or in whom cardioversion is planned.

19.          Dr Rajnish Sardanna: Dronedarone should NOT be prescribed exclusively as a rate control medication and the results of the PALLAS trial, which demonstrated an increase in cardiovascular mortality when dronedarone was used solely as a rate controlling agent.

20.          Dr Rajnish Sardanna: Dronedarone is only rarely effective for the chemical cardioversion of AF or atrial flutter to sinus rhythm (less than 10 percent of patients). As such, dronedarone should NOT be used for this purpose.

21.          Dr Rajnish Sardanna: FDA warning has been issued in 14.1.11 and 21.7 11

22.          Dr A K Omar: Early initiation of dual antiplatelet therapy with aspirin and either a P2Y12 receptor blocker or GP IIb/IIIa inhibitor helps in all patients with non-ST elevation ACS, whether they are managed by a conservative or an invasive strategy.

23.          Dr A K Omar: For all patients with non-ST elevation ACS, give dual anti platelet therapy with aspirin 300mg and a P2Y12 receptor blocker.

24.          Dr A K Omar: The loading dose for ticagrelor is 180 mg, for prasugrel 60 mg, and for clopidogrel 300-600 mg.

25.          Dr A K Omar: For those patients with a history of gastrointestinal bleeding, drugs which reduce the risk of recurrent bleeding (eg, proton pump inhibitors) should be given.

26.          Dr A K Omar: For those patients scheduled for an early invasive approach, we recommend giving either ticagrelor (at presentation) or prasugrel (with definition of coronary anatomy), as opposed to clopidogrel

27.          Dr A K Omar: For those patients who are managed with a delayed invasive approach (coronary angiography after four hours), start ticagrelor (at presentation) instead of clopidogrel and suggest ticagrelor instead of prasugrel (with definition of coronary anatomy)

28.          Dr A K Omar: For those patients managed without an invasive approach (conservative approach), start ticagrelor as opposed to clopidogrel

29.          Dr A K Omar: Give indefinite aspirin for all patients with non-ST elevation acute coronary syndromes

30.          Dr A K Omar: Give clopidogrel (75 mg/day) or prasugrel (10 mg for patients ≥60 kg) or ticagrelor 90 mg twice daily for at least one year in all patients with non-ST elevation ACS

31.          Dr Subhash Chandra: Apixaban or rivaroxaban in atrial fibrillation — Apixaban and rivaroxaban are two newer oral anticoagulants that do not require laboratory monitoring. In two randomized trials in patients with atrial fibrillation that compared one of these drugs to warfarin, ARISTOTLE and ROCKET-AF, apixaban and rivaroxaban (respectively) met the criteria for non-inferiority for the lowering of the risk of stroke and systemic embolization. Based on these two trials, and the results of the older RE-LY trial of dabigatran, one should sue a direct thrombin inhibitor or a factor Xa inhibitor rather than warfarin in patients with atrial fibrillation who require anticoagulation.

32.          Dr Sandeep Bansal: The World Health Organization (WHO) classifies patients with pulmonary hypertension (PH) into five groups based upon etiology. Patients in the first group are considered to have pulmonary arterial hypertension (PAH), whereas patients in the remaining four groups are considered to have PH

33.          Dr Sandeep Bansal: Vasoreactivity test — It is recommended that patients with group 1 PAH undergo a vasoreactivity test. This involves the administration of a short-acting vasodilator and then measurement of the hemodynamic response using a right heart catheter. Agents commonly used for vasoreactivity testing include epoprostenol, adenosine, and inhaled nitric oxide:

Epoprostenol is infused at a starting rate of 1 to 2 ng/kg per min and increased by 2 ng/kg per min every 5 to 10 minutes until a clinically significant fall in blood pressure, an increase in heart rate, or adverse symptoms (nausea, vomiting, headache) develop.

Adenosine is administered intravenously in doses of 50 mcg/kg per min and increased every two minutes until uncomfortable symptoms develop or a maximal dose of 200 to 350 mcg/kg per min is reached

Inhaled nitric oxide administered at 10 to 20 ppm is selective for the pulmonary vasculature.

An acute vasoreactivity test is considered positive if mean pulmonary artery pressure decreases at least 10 mmHg and to a value less than 40 mmHg, with an increased or unchanged cardiac output, and a minimally reduced or unchanged systemic blood pressure. Patients with a positive vasoreactivity test are candidates for a trial of CCB therapy with a dihydropyridine or diltiazem.

34.          Dr Praveen Chandra: A number of newer medical and invasive therapies have been evaluated for use in patients with stable angina. Of these, only ranolazine, a late sodium channel blocker, has been approved for clinical use and its role is evolving

35.          Dr Praveen Chandra: Ranolazine can be used as an option for angina patients who have failed all other anti anginal therapies. The initial dose of ranolazine is 500 mg twice daily. For patients who remain symptomatic, 1000 mg twice daily may be used.

36.          Dr Praveen Chandra: Ivabridine  is a novel agent that acts specifically on the sinus node ionic channels to slow the heart rate. There is no effect on blood pressure, conduction, or cardiac contractility. This results in isolated slowing of the pulse and consequent improvement in angina threshold without the side effect of depression, cardiac function, or potentially increasing atrio-ventricular block

37.          Dr Praveen Chandra: Stable angina pectoris, or stable angina, refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin.

38.          Dr Praveen Chandra: The goals of treatment of stable angina involve therapies to prevent/minimize ischemia and to improve survival. These goals can be achieved with a variety of modalities including medical therapy, non pharmacologic and lifestyle measures, and revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG).

39.          Dr Praveen Chandra: In chronic stable angina there are two primary indications for coronary angiography followed by revascularization of appropriate lesions: Angina that significantly interferes with a patient’s lifestyle despite maximal tolerable medical therapy and patients with high-risk criteria and selected patients with intermediate-risk criteria on noninvasive testing, regardless of anginal severity.

40.          Dr Praveen Chandra: Revascularization is performed in appropriate patients in whom angiography reveals anatomy for which revascularization has a proven benefit or in whom medical therapy has failed.

41.          Dr Praveen Chandra: The choice between PCI and CABG is based upon anatomy and other factors such as left ventricular function and the presence or absence of diabetes. With the availability of drug-eluting stents, PCI is increasingly performed for most lesions.

42.          Dr U Kaul: Prospective trials have demonstrated that fibrinolytic therapy is not beneficial in patients with a non-ST elevation ACS

43.          Dr U Kaul: TIMI risk score: Outcome in patients with unstable angina or an NSTEMI; a value of one was assigned when a factor was present and 0 when it was absent.

•             Age ≥65 years

•             Presence of at least three risk factors for CHD (hypertension, diabetes, dyslipidemia, smoking, or positive family history of early MI)

•             Prior coronary stenosis of ≥50 percent

•             Presence of ST segment deviation on admission ECG

•             At least two anginal episodes in prior 24 hours

•             Elevated serum cardiac biomarkers

•             Use of aspirin in prior seven days (which is probably a marker for more severe coronary disease)

Patients are considered to be at low risk with a score of 0 to 1; intermediate risk with a score of 2 to 3; and high risk with a score of 4 to 7.

44.          Dr U Kaul: Bad prognosis markers: St depression, positive troponin and low estimated GFR

45.          Dr U Kaul: In angina there are three presentations of angina that suggest an acute coronary syndrome (ACS):Rest angina, which is usually more than 20 minutes in duration; New onset angina that markedly limits physical activity and Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina

46.          Dr U Kaul: UA and NSTEMI differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (troponins): UA is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins. NSTEMI is considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present

47.          Dr U kaul: Since an elevation in troponins may not be detectable for hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation. As a consequence, initial management is the same for these two syndromes.

48.          Dr U Kaul: The 2007 ACC/AHA guidelines has concluded that anticoagulant therapy should be added to anti platelet therapy in most patients with ACS

49.          Dr U Kaul: For patients managed with an invasive approach, UFH, enoxaparin, bivalirudin, and fondaparinux all have established efficacy.

50.          Dr U Kaul: For patients managed with a conservative strategy, enoxaparin, UFH, or fondaparinux are recommended. Fondaparinux is better.

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