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.