SHIFT - Ivabradine for heart failure with reduced ejection fraction

Swedberg K, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): A randomised placebo-controlled study. Lancet 2010;376:875-85.

Bottom-line: In patients with HFrEF and a resting heart rate >70 bpm despite maximally-tolerated beta-blocker therapy, ivabradine reduced the risk of hospital admissions (NNT 25), mainly by reducing HF-related hospitalization, over ~2 years.

When using ivabradine, monitoring HR via pulse and EKG at baseline and at follow-up is critical to ensure benefit, and to minimize symptomatic bradycardia (NNH 25) and atrial fibrillation (NNH 100). It appears that the higher the baseline HR, the greater the benefit (and likely the lower risk of bradycardia).

 

Patients (n=6558)

  • Inclusion

    • Age 18+ y

    • Stable symptomatic HF for at least 4 weeks

    • LVEF 35% or lower

    • HF hospitalization in the last 12 months

    • Normal sinus rhythm with HR 70+ bpm on 12-lead EKG after 5 min of rest on 2 consecutive visits

  • Exclusion

    • HF etiology of congenital heart disease or primary severe valvular disease

    • MI in last 2 months

    • CRT implanted in last 6 months

    • Implantable pacemaker that's pacing >40% of the day

    • Permanent AF/flutter

    • Symptomatic hypotension

    • Drugs: Use of diltiazem or verapamil, class I antiarrhythmics or strong CYP 3A4 inhibitors

  • Screened 7411 -> randomized 6558

  • "Average" patient in the trial

    • Age 60 y

    • Male 76%

    • Duration of HF 3.5 y

    • HF etiology: Ischemic 68%

    • NYHA class: II (~50%), III (~50%)

    • PMHx

      • MI 56%

      • HTN 67%

      • Diabetes 30%

      • AF/flutter 8%

    • BP 122/76 mm Hg

    • HR 80 bpm

    • LVEF 29%

    • eGFR 75 mL/min*1.73 m^2

    • Meds

      • Beta-blocker ~90% (26% on target dose, 56% on at least 1/2 target dose)

      • ACEI ~80%, ARB 14%

      • Mineralocorticoid antagonist ~60%

      • Diuretic 84%

      • Digoxin 22%

      • Devices: ICD 3%, CRT 1%

Intervention & control

  • I: Ivabradine

    • Initial dose of 5 mg PO BID

    • After 14 days:

      • If HR >60 bpm, increased to 7.5 mg PO BID

      • If HR 50-60 bpm, kept on 5 mg PO BID

      • If HR <50 bpm or symptomatic bradycardia, dose reduced to 2.5 mg PO BID

    • At each subsequent follow-up, above algorithm used to titrate between 2.5-7.5 mg PO BID

  • C: Matching placebo

Results @ median 1.9 years

  • HR

    • @ 1 month: Ivabradine 64 bpm, placebo 75 bpm

    • @ 2-3 years: 67 vs 75 bpm

  • Significant reduction with ivabradine in:

    • Serious adverse events: Ivabradine 45%, placebo 48% (p=0.025)

    • Primary outcome (CV death or hospital admission for HF): 24% vs 29% (hazard ratio 0.82, 0.75-0.90), NNT 20

    • Hospital admission: 38% vs 42% (HR 0.90, 0.82-0.96), NNT 25

      • For HF: 16% vs 21%

    • Unclear effect on death

      • No statistically significant difference in death (16% vs 17%. HR 0.90, 0.80-1.02) or CV death: 14% vs 15% (HR 0.91, 0.80-1.03)

      • Reduction in death from HF: 3% vs 5% (HR 0.74, 0.58-0.94)

    • Significant increase with ivabradine in:

      • Symptomatic bradycardia: 5% vs 1%, NNH 25

      • Asymptomatic bradycardia: 6% vs 1%, NNH 20

      • Atrial fibrillation: 9% vs 8%, NNH 100

      • Blurred vision: 1% vs <1%, NNH 100

      • Phosphenes: 3% vs 1%, NNH 50

  • Subgroup analyses demonstrated a significant interaction between baseline HR 77 bpm or greater versus <77 bpm and effect on the primary outcome. Greater relative benefit was seen in patients with a higher baseline HR.

Generalizability

  • Patients included in this trial overall had HFrEF of ischemic and non-ischemic origin with NYHA functional class II or III

  • Use of background medical therapies for HFrEF was fairly good, although very few patients were optimized on beta-blockers, with the most common reasons cited as hypotension and fatigue

Internal validity

  • Low risk of allocation, performance and detection bias

    • Computer-generated randomization with central, automated allocation and blinding with use of identical placebo)

  • Low risk of attrition bias

    • Loss-to-follow-up <1%

    • Intention-to-treat analysis

Other studies

  • The BEAUTIFUL trial, which came out before SHIFT, evaluated the use of ivabradine in patients with CAD and LV dysfunction with a heart rate of 60 bpm or greater

    • Patients were quite similar to those in the SHIFT trial with a mean HR of 72 bpm and 84% with HFrEF NYHA class II or III

    • In the overall population studied in BEAUTIFUL, ivabradine did not reduce the risk of CV events

    • In a subgroup of patients with HR >70 bpm (mimicking the SHIFT population), there was no reduction in the primary outcome or any HF-related outcome.

  • A pooled analysis of BEAUTIFUL and SHIFT showed results consistent with the SHIFT trial in patients with HFrEF and HR of 70 bpm or more.

  • The SIGNIFY trial, which was published after SHIFT, evaluated ivabradine in patients with CAD without HF with a HR of 70 bpm or greater

    • Patients had stable CAD, no HF, a mean HR of 77 bpm, and a mean LVEF of 56%

    • All analyses of SIGNIFY demonstrated no benefit on CV outcomes, with a possible increase in HF-related hospital admission (HR 1.20, 0.99-1.46), and an increased risk of the primary CV outcome in patients with angina CCS class II-IV at baseline

    • In this population, ivabradine increased the risk of adverse events (NNH 14), symptomatic bradycardia (NNH 15), phosphenes (NNH 20) and blurred vision (NNH 125)

    • SIGNIFY therefore solidifed that ivabradine has no role in CAD without HF.

  • None of the trials (BEAUTIFUL, SHIFT, SIGNIFY) enrolled patients with HFpEF. The role of ivabradine in HFpEF is therefore unknown.

 

 

Association between serum triglycerides (non-fasting) & pancreatitis

Pedersen SB, et al. Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis. JAMA Intern Med 2016

Bottom-line: Serum triglyceride concentrations increase the risk of pancreatitis in a "dose-dependent" manner (i.e. the higher the concentration, the greater the risk).

The absolute risk increase of mild-moderate triglyceride elevations remains small. With a risk of pancreatitis of ~1% over 10 years, individuals with a triglyceride concentration of ~5-10 mmol/L are unlikely to benefit from medical management to lower triglycerides (e.g. fibrates).

 

Design summary

  • Registry-based cohort study conducted in the Netherlands.
  • Patients: Included 116,550 individuals, 434 of whom developed acute pancreatitis (0.3%) over a median 6.7 years of follow-up.
  • Exposure: Non-fasting serum triglyceride concentration, separated into 6 categories ranging from <1 mmol/L to 5+ mmol/L.
    • Individuals with a triglyceride concentration 5+ mmol/L represented <2% of the general population in this study.
  • Co-variables included age, sex, BMI, alcohol intake/week, education level, smoking status, hypertension, diabetes, statin use, birth year, HDL.
  • Outcome: Death or hospitalization with ICD-8/10 code for acute or chronic pancreatitis.

Results

  • Adjust events per 10,000 person-years based on serum triglyceride concentration (hazard ratio, 95% confidence interval versus <1.00 mmol/L):
    • <1.00 mmol/L: 2.7 = 0.3% over 10 years
    • 1-1.99 mmol/L: 4.3 (HR 1.7, 1.0-2.7)
    • 2-2.99 mmol/L: 5.5 (HR 2.4, 1.4-4.2)
    • 3-3.99 mmol/L: 6.3 (HR 3.2, 1.6-6.5)
    • 4-4.99 mmol/L: 7.5 (HR 4.6, 1.8-12)
    • 5 mmol/L or greater: 12 = 1.2% over 10 years (HR 11, 4.7-26)

Additional observations

  • Previous smaller studies showed that triglyceride concentrations needed to be >20 to >34 mmol/L in order to significantly increase the risk of acute pancreatitis

AF-CHF - Rhythm vs rate control in AF with HFrEF

Roy D, et al. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med 2008;358:2667-77.

Bottom-line: In individuals with both AF & HFrEF, a rhythm-control strategy is not superior to an aggressive rate-control strategy targeting resting HR <80 bpm. More patients starting with the rhythm-control strategy will require a strategy change (NNH 9), but neither strategy works for everybody.

 

Patients (n=1376)

  • Inclusion
    • AF
      • Episode with EKG documentation lasting at least 6h or requiring cardioversion in previous 6 months, or
      • Episode lasting 10+ minutes in previous 6 months & previous cardioversion for AF
    • HF
      • NYHA II-IV in previous 6 months, or
      • Hospitalized for HF in previous 6 months, or
      • LVEF 25% or less
    • LVEF 35% or less measured in last 6 months
  • Exclusion
    • Persistent AF >12 months
    • Reversible cause of AF or HF
    • Decompensated HF in previous 48h
    • Use of antiarrhythmics for other arrhythmias
    • 2o-3o AVB with bradycardia <50 bpm
    • Hx long QT syndrome
    • Dialysis-dependent renal failure
  • "Typical" patient
    • Age 66 y
    • Male 78-85%
    • NYHA class III-IV 32%
    • HF etiology: Ischemic (48%), hypertensive (10%), valvular (5%)
    • Prior hospitalization for AF (50%), HF (55%)
    • AF paroxysmal (1/3), persistent (2/3)
    • PMHx
      • Previous stroke/TIA 10%
      • HTN 49%
      • Diabetes 22%
    • AF on EKG (55-60%)
    • LVEF 27%
    • Concomitant meds
      • ACEI 86%, ARB 11%
      • Mineralocorticoid antagonist 45%
      • OAC 85-90%
      • ASA 40%
      • Lipid-lowering 43%
    • ICD 7%

Interventions

  • I: Rhythm control: Aggressive pharmacotherapy + electrical cardioversion to prevent and cardiovert AF
    • Drug of choice: Amiodarone, then sotalol or dofetilide as required
    • Drugs @ 1 year: Amiodarone (82%), sotalol (2%), dofetilide (<1%)
      • Beta-blocker (80%), digoxin (~50%), anticoagulant (88%)
    • Electrical cardioversion
      • 1st recommended <6 weeks after enrollment not converting to NSR with pharmacological rhythm control alone
    • 2nd recommended <3 months after enrollment if still not in NSR
    • Subsequent cardioversions PRN
  • C: Rate control: Adjusted doses of beta-blocker & digoxin to achieve resting HR <80 bpm & <110 bpm during 6-min walk test (tested @ month 4 & 12, then yearly)
    • Drugs @ 1 year: Beta-blocker (88%), digoxin (75%), verapamil/diltiazem (3%)
      • Amiodarone (7%), sotalol or dofetilide (<1%), anticoagulant (92%)
  • Interventions common to both groups:
    • Max-tolerated doses of beta-blockers (for HFrEF management)
    • Anticoagulation

Results @ mean 3 y f/u

  • Death: 32% vs 33% (p=0.68)
    • CV death (primary outcome): 27% vs 25% (p=0.53)
  • Hospitalization: 64% vs 59% (p=0.06)
    • AF hospitalization: 14% vs 9% (p=0.001)
  • Worsening HF: 28% vs 31% (p=0.17)
  • Switched to other intervention: 21% vs 10%
  • AF on EKG at study visit:
    • Month 4, years 1-3: ~20% vs ~60% (during f/u, >55% in rhythm-control group had at least 1 AF recurrence)
    • Year 4: ~25% vs ~70%

Generalizability

  • Representative of individuals with HFrEF and moderately good use of HFrEF medical therapies & low ICD use
  • Rhythm-control intervention consistent with real world use; rate-control intervention similar to "intensive" intervention from AFFIRM trial

Internal validity

  • Unclear risk of allocation bias
    • Allocation concealment not described + some moderately-large baseline differences in certain characteristics (e.g. male 78% vs 85%, AF on baseline EKG 54% vs 61%)
  • Unclear risk of performance & detection bias
    • Predefined treatment protocols accounted for most potential differences in interventions
    • Rhythm-control group required more AF-related hospitalizations, likely cardioversion-related
    • Higher rate of cross-over in rhythm-control group
    • Once outcomes reported, adjudicated by committee unaware of treatment allocation
  • Unclear risk of attrition bias
    • 5-6% loss-to-follow-up, which could be enough to hide differences between groups in main outcomes

BP lowering: High-dose monotherapy or low-dose combo?

Law MR, et al. Value of low dose combination treatment with blood pressure lowering drugs: Analysis of 354 randomised trials. BMJ 2003;326:1427.

Bottom-line: In patients with hypertension, addition of an extra BP-lowering agent at a low dose provides greater BP-lowering with fewer side effects than increasing the dose of a single agent.

Each additional low-dose BP-lowering drug reduces BP by an extra ~6/3 mm Hg & cause side effects in an extra 1 out of every ~50 people. Conversely, doubling the dose of a BP-lowering agent will further reduce BP by ~2/1 mm Hg & cause side effects in an extra 1 out of every 12-30 people.

 

Design summary

  • Systematic review with meta-analysis of 354 randomized controlled trials (RCTs) including 39,879 patients receiving active treatment & 15,817 receiving placebo
    • Databases searched: MEDLINE, Cochrane Library, Web of Science
    • Search date: Unclear (before June 2003)
    • Study eligibility criteria: Double-blind RCTs of at least 2-weeks duration evaluating dose response + effect of combination of antihypertensives

Patients & interventions

  • Key baseline characteristics
    • Age, mean: 53 y
    • BP, median: 154/97 mm Hg
  • Drug classes included: ACE inhibitors, ARBs, beta-blockers, calcium-channel blockers, thiazide diuretics

Outcomes at 2-12 weeks

  • BP lowering (similar across all 5 drug classes at comparable doses)
    • By dose
      • 1/2 standard dose: ~7/4 mm Hg
      • Standard dose (defined as typical maintenance dose based on British National Formulary, e.g. amlodipine or ramipril 2.5 mg/d): ~9/6 mm Hg
      • Double standard dose: ~11/7 mm Hg
      • In other words, doubling the dose of BP-lowering therapy further lowered BP by ~2/1 mm Hg
    • By # of drugs from different classes at 1/2 standard dose
      • 1 drug: ~7/4 mm Hg
      • 2 drugs: 13/7 mm Hg
      • 3 drugs: 20/11 mm Hg
      • In other words, BP-lowering drugs have additive efficacy
  • % with adverse effects
    • By class based on dose
      • ACE inhibitor: ~4% at all doses
      • ARB: ~0-2% at all doses
      • Beta-blocker
        • 1/2 standard dose: ~5-6%
        • Standard dose: ~7-8%
        • Double standard dose: ~9-10%
      • Calcium-channel blocker
        • 1/2 standard dose: 2%
        • Standard dose: 8%
        • Double standard dose: 15%
      • Thiazide diuretic
        • 1/2 standard dose: 2%
        • Standard dose: 10%
        • Double standard dose: 18%
    • By # of drugs
      • 1 drug: ~5%
      • 2 drugs: 7-8%
      • 3 drugs: Not studied

WARCEF - Warfarin vs ASA in HFrEF in sinus rhythm

Homma S, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med 2012;366:1859-69.

Bottom-line: In patients with HFrEF in sinus rhythm and without any additional risk factors for cardiac embolism, warfarin reduced the risk of ischemic stroke, and increased the risk of major and minor hemorrhages and HF hospitalization (possibly from anemia or cessation/reduction of HF meds during bleeding events).

For every 1000 patients with HFrEF in sinus rhythm, treatment warfarin instead of ASA would result in 7 fewer ischemic strokes, 11 extra HF hospitalizations, 9 extra major and 43 extra minor bleeds per year. Thus for most patients represented here, the risks far outweigh the benefits.

 

Patients (n=2305)

  • Inclusion
    • Age 18+ y
    • HFrEF
      • NYHA class I-IV
      • LVEF 35% or less assessed in the past 3 months
    • Normal sinus rhythm
    • Modified Ranking scale (mRS) <5 (i.e. no more than moderately severe disability)
    • Planned treatment with a beta-blocker plus ACEI/ARB/hydralazine+nitrate
  • Exclusion:
    • Clear indication for either warfarin or ASA
    • High risk of cardiac embolism
      • AF
      • Mechanical heart valve
      • Endocarditis
      • Intracardiac thrombus (mobile or pedunculated)
  • Screened ? -> randomized & analyzed 2305
  • Typical trial patient
    • Age 61 y
    • Male 80%
    • North American ~50%
    • NYHA class I (14%), II (55%), III (30%), IV (~1%)
    • mRS 0 (41%), 1 (31%), 2 (23%), 3-4 (5%)
    • Ischemic HF etiology 43%
    • PMHx
      • Stroke/TIA 13%
      • MI 48%
      • Current smoker 17%
      • ETOH consumption >2 onces/day - 25%
      • HTN 61%
      • Diabetes 32%
      • AF 4%
    • BMI 29
    • BP 124/74 mm Hg
    • HR 72 bpm
    • LVEF 25%
    • Meds
      • ACEI/ARB 98%
      • Beta-blocker 90%
      • Mineralocorticoid antagonist 60%
      • Diuretic 80%
      • Nitrate 25%
      • Statin 83%
      • Prior to randomization: ASA (59%), other antiplatelet (7%), oral anticoagulant (8%)
    • ICD 18%

Interventions

  • Warfarin with target INR 2.75 (range 2.0 to 3.5)
    • Mean INR during trial 2.5 +/- 1, time in target range=63%
    • Spent 66% of follow-up on study treatment
  • ASA 325 mg PO once daily
    • Spent 68% of follow-up on study treatment

Results @ mean 3.5 y

  • No statistically significant difference in
    • Primary outcome (death, ischemic stroke, intracerebral hemorrhage): Warfarin 26.4% vs ASA 27.5%, hazard ratio (HR) 0.93 (95% confidence interval 0.79-1.10)
    • Secondary outcome (primary outcome, MI, HF hospitalization): 39.1% vs 37.4%, HR 1.07 (0.93-1.23)
    • Death: 23.5% vs 22.6%
  • Statistically significant
    • Reduction with warfarin in
      • Ischemic stroke: 2.5% vs 4.7%, HR 0.52 (0.33-0.82, NNT 46)
        • Per year: 0.7% vs 1.4% (NNT 143/year)
    • Increase with warfarin in
      • HF hospitalization: 20.9% vs 17.5%, HR 1.21 (1.00-1.47, NNH 30)
        • Per year: 6.8% vs 5.7% (NNH 91/year)
      • Major hemorrhage: 1.8%/year vs 0.9%/year, HR 2.05 (1.36-3.12, NNH 112/year)
      • Minor hemorrhage: 11.6%/year vs 7.3%/year, HR 1.56 (1.34-1.81, NNH 24/year)

Generalizability

  • The study population represents a typical HFrEF population of both ischemic & non-ischemic etiology with good to excellent use of background therapy for systolic dysfunction
    • 43% of patients had ischemic cardiomyopathy, therefore qualifying for ASA for secondary prevention
    • 57% had non-ischemic cardiomyopathy, for which antiplatelet therapy would not be indicated routinely. Since this trial has no placebo group, it's not able to answer whether these patients need any antithrombotic therapy at all in the absence of another indication.
  • The target INR in this trial (2.75, range 2.0-3.5) was higher than typically used in practice for AF (2.5, range 2.0-3.0), but similar to that used for mechanical mitral or high-risk aortic valves (3.0, range 2.5-3.5), however the mean INR during the trial was 2.5. Similarly, the ASA dose (325 mg/d) was higher than that typically used for AF/secondary prevention (75-100 mg/d). Thus, bleeding in both groups is likely to be higher than with regimens used in practice, particularly in the ASA group.

Issues with internal validity?

  • No: Centrally randomized, allocation-concealed, double-dummy double-blind trial with blinded outcome adjudication, and low loss-to-follow-up (1.5%) analyzed using intention-to-treat population.

Other studies

  • 3 other RCTs (WASH 2004, HELAS 2006, WATCH 2009) with a total of 1358 patients compared warfarin to ASA in patients with HF. Meta-analysis of all 4 trials demonstrates results consistent with WARCEF: Warfarin cut the risk of ischemic stroke by ~half, & ~doubled the risk of major & minor bleeds compared to ASA.