6/24/2013 1 What’s New In Interventional Cardiology Yerem Yeghiazarians, MD Yerem Yeghiazarians, M.D. Leone-Perkins Family Endowed Chair in Cardiology University of California, San Francisco June 24, 2013 Yerem Yeghiazarians, MD Disclosures: No conflicts of interest Today’s Topics Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD? Case 2: When to look for and treat secondary hypertension due to renal artery disease? Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis? Today’s Topics Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD? Case 2: When to look for and treat secondary hypertension due to renal artery disease? Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis?
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6/24/2013
1
What’s New In Interventional Cardiology
Yerem Yeghiazarians, MD
Yerem Yeghiazarians, M.D.Leone-Perkins Family Endowed Chair in Cardiology
University of California, San FranciscoJune 24, 2013
Yerem Yeghiazarians, MDDisclosures:
No conflicts of interest
Today’s Topics
Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD?
Case 2: When to look for and treat secondary hypertension due to renal artery disease?
Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis?
Today’s Topics
Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD?
Case 2: When to look for and treat secondary hypertension due to renal artery disease?
Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis?
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Case 1 – Mr. C.N.
• 78 y.o. man very active male with reported cardiac risk factors of HTN, HL, and pre-diabetes who presented with progressive exertional chest pain x 1 month. Saw his PCP and referred to a referring cardiologist (4/2013).
Physical Exam
• BP 115/75; HR 64; RR 12; O2sat 98% on RA
• Gen: NAD, AAOx3
• Neck: JVP flat
• Chest: CTAB
• CV: RRR, normal S1/S2, no m/g/r
• Abd: soft, NTND, no abdominal bruit
• Ext: no edema, warm ext
Mr. C. N.
• No cardiac meds
• EKG with RBBB
• CXR normal
• Labs at baseline normal
• Lipids –TC 217, LDL 132, HDL 43, TG 208
• Bruce protocol, 6’05”, 7.1 METS, 8-9/10 chest pain at peak exercise, ST depression 0.75 mm V2-6
– Ischemia entire septum as well as mid-distal anterior wall to apex
– EF dropped from 50% to 20%
– LV cavity enlarged with stress compared with rest
Stress Myocardial Perfusion
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How would you manage him next?
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3% 3%
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A. Start aspirin, beta-blocker and treat symptoms with nitrates
B. Start aspirin, beta-blocker, statin and see how he does
C. Start aspirin, beta-blocker, statin and refer for cardiac cath
D. Start aspirin, beta-blocker and get a stress echocardiogram
• Decision was made by his PCP and referring Cardiologist, presumably based on the Courage Trial, to treat medically
• Aspirin, Metoprolol 25mg BID, Imdur 30mg QD
When not to say you are following the
COURAGE Trial?
This is a good example
COURAGE TRIAL
• 2,287 patients in US and Canada
• Coronary artery disease documented by coronary angiography + ischemia
• Randomized to optimal medical therapy (OMT) or PCI +OMT (PCI)
Boden et al NEJM 2007
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COURAGE TRIAL
Inclusion criteria:• ≥ one 70% stenosis +
abnormal ECG /positive stress test
OR• ≥ one 80% stenosis +
angina
Exclusion criteria• CCS class IV angina• Markedly positive stress
• Of the >35,000 patients screened, only ~2,287 were eligible and randomized (~6%)– Not your “real world practice”
• 42% of patients had class 0 or 1 angina at baseline
• 33% of OMT group had PCI or CABG
• Drug eluting stents in only ~3% • All patients had a cardiac cath to define the
anatomy firstShaw, L. J. et al. Circulation 2008;117:1283-1291
COURAGE Nuclear Substudy
Ischemia Reduction and Outcome
Cum
ulat
ive
Eve
nt-F
ree
Sur
viva
l
Findings suggest a treatment target of ≥5% ischemia reduction
When to get concerned about stress test
findings?
Typical angina Atypical angina
Non-anginalchest pain
AGE Men Women Men Women Men Women
30-39 69.7 25.8 21.8 4.2 5.2 0.8
40-49 87.3 55.2 46.1 13.3 14.1 2.8
50-59 92.0 79.4 58.9 32.4 21.5 8.4
60-69 94.3 90.6 90.6 54.6 28.1 18.6
Diamond, Forrester et al JCI 1980
Pre-test Probability of CAD
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• Early positive-stage I: Mortality >5%/year• Strongly positive > 2.5 mm ST depression• ST elevation > 1 mm in leads without Q waves• Fall in SBP >10 mm Hg• Early onset ventricular arrhythmias• Chronotropic incompetence (HR <120/min not
due to drugs)• Prolonged ischemic changes in recovery
> 2mm lasting > 6 minutes in multiple leads
High Risk Features on Stress Testing Prognostic Information -- Stress Testing Duke treadmill score = duration of exercise in minutes on the Bruce protocol- (minus) 5x maximal mm ST deviation- (minus) 4x treadmill angina index
Angina score:0 if no angina.1 if non-limiting angina.2 if limiting angina.
High Risk < -10 79% 4-year survivalModerate Risk -10 to +4 95% 4-year survivalLow Risk >+5 99% 4-year survival
Mark et al, Ann Int Med 1987
Prognostic Information -- Stress Testing Duke treadmill score = duration of exercise in minutes on the Bruce protocol- (minus) 5x maximal mm ST deviation- (minus) 4x treadmill angina index
Angina score:0 if no angina.1 if non-limiting angina.2 if limiting angina.
High Risk < -10 79% 4-year survivalModerate Risk -10 to +4 95% 4-year survivalLow Risk >+5 99% 4-year survival
Mark et al, Ann Int Med 1987
Our patient:
6 – 5 (0.75) – 4 (2) = - 5.75
• Large defect
• Multiple moderate defects
• LV dilation or increased lung thaliumuptake indicating low cardiac output or elevated LVEDP
• Echo abnormal in >2 segments at low dose dobutamine or low heart rate (<120 bpm)
• Drop in LVEF
High Risk Features on Stress Testing
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• Bruce protocol, 6’05”, 7.1 METS, 8-9/10 chest pain at peak exercise, ST depression 0.75 mm V2-6
– Ischemia entire septum as well as mid-distal anterior wall to apex
– EF dropped from 50% to 20%
– LV cavity enlarged with stress compared with rest
• LV dilation or increased lung thaliumuptake indicating low cardiac output or elevated LVEDP
• Drop in LVEF
High Risk Features on Stress TestingOur patient
This patient would have been excluded from the
Courage Trial – he has very high risk features and you
need to define his anatomy
A) Start aspirin, beta-blocker and treat symptoms with nitrates
B) Start aspirin, beta-blocker, statin and see how he does
C) Start aspirin, beta-blocker, statin and refer for cardiac cath
D) Start aspirin, beta-blocker and get a stress echocardiogram
How would you manage him next?
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GNL 2011GNL 2011 GNL 2011
Anatomy RevascMethod
COR LOE
3 VD +/- Proximal LAD Disease*#
CABG I BPCI IIbOf uncertain benefit B
2 VD With Proximal LAD Disease#
CABG I BPCI IIbOf uncertain benefit B
2 VD Without Proximal LAD Disease#
CABG IIaWith extensive ischemia BIIbOf uncertain benefit without extensive
ischemiaC
PCI IIbOf uncertain benefit B1 VD With Proximal LAD disease
CABG IIaWith LIMA for long-term benefit BPCI IIbOf uncertain benefit B
1 VD WithoutProximal LAD disease
CABG III: Harm BPCI III: Harm B
*Reasonable to choose CABG over PCI for good CABG candidates with complex 3-vessel disease (e.g., SYNTAX score >22) (Class IIa; LOE:B)
#Reasonable to choose CABG over PCI for MVD in patients with DM (Class IIa; LOE:B)
Revascularization to Improve Survival
GNL 2011
• Left Main disease• Survivors of sudden cardiac death with
presumed ischemia-mediated VT
GNL 2011
Anatomy RevascMethod
COR LOE
3 VD +/- Proximal LAD Disease*#
CABG I BPCI IIbOf uncertain benefit B
2 VD With Proximal LAD Disease#
CABG I BPCI IIbOf uncertain benefit B
2 VD Without Proximal LAD Disease#
CABG IIaWith extensive ischemia BIIbOf uncertain benefit without extensive
ischemiaC
PCI IIbOf uncertain benefit B1 VD With Proximal LAD disease
CABG IIaWith LIMA for long-term benefit BPCI IIbOf uncertain benefit B
1 VD WithoutProximal LAD disease
CABG III: Harm BPCI III: Harm B
*Reasonable to choose CABG over PCI for good CABG candidates with complex 3-vessel disease (e.g., SYNTAX score >22) (Class IIa; LOE:B)
#Reasonable to choose CABG over PCI for MVD in patients with DM (Class IIa; LOE:B)
Revascularization to Improve Survival
GNL 2011
• Left Main disease• Survivors of sudden cardiac death with
presumed ischemia-mediated VT
GNL 2011
Revascularization to Improve SymptomsClinical Setting COR LOE
≥1 significant stenoses amenable to revascularization and unacceptable angina despite GDMT
I−CABG AI−PCI
≥1 significant stenoses and unacceptable angina in whom GDMT cannot be implemented because of medication contraindications, adverse effects, or patient preferences
IIa−CABG CIIa−PCI
Previous CABG with ≥1 significant stenoses associated with ischemia and unacceptable angina despite GDMT
IIb-CABG CIIa−PCI C
Complex 3 VD (e.g., SYNTAX score >22) +/-involvement of the proximal LAD and a good candidate for CABG
IIa−CABG preferred over PCI
B
No anatomic or physiologic criteria for revascularization
III: Harm−CABG CIII: Harm−PCI
GNL 2011
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Case 1: Back to Mr. C. N.
• 4 days later, he continued to have persistent symptoms and comes to UCSF ER
• EKG with RBBB and NSSTT waves
• Troponin 0.72 (nl <0.05 µg/L)
• Treated with aspirin 325 mg, Clopidogrel 600 mg, and started on IV Heparin
• Persistent on/off chest pains
• Cardiology consulted
• Cardiac cath recommended for ACS
New clinical classification of MIClassification Description1 Spontaneous MI related to ischemia due to a
primary coronary event, such as plaque erosion and/or rupture, fissuring, or dissection
2 MI secondary to ischemia due to an imbalance of O2supply and demand, as from coronary spasm or embolism, anemia, arrhythmias, hypertension, or hypotension
3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggesting ischemia with new ST-segment elevation; new left bundle branch block; or pathologic or angiographic evidence of fresh coronary thrombus--in the absence of reliable biomarker findings
4a MI associated with PCI4b MI associated with documented in-stent thrombosis5 MI associated with CABG surgery
Thygesen K et al. Circulation 2007; available at: http://circ.ahajournals.org.
GNL 2011
General Considerations in Deciding Between an Early Invasive Strategy and an Initial Conservative Strategy in UA/NSTEMI
Early Invasive Strategy Generally Preferred
Initial Conservative Strategy Generally Preferred or Reasonable
• Recurrent angina or ischemia at rest or with low level activities despite intensive medical therapy
• Elevated cardiac biomarkers (TnT or TnI)• New or presumably new ST-depression • Signs or symptoms of heart failure• Hemodynamic instability• High risk score (e.g., GRACE, TIMI)• Sustained ventricular tachycardia• PCI within 6 mo• Prior CABG• Diabetes mellitus• Mild to moderate renal dysfunction• Reduced LV function (LVEF <40%)
• Low risk score (e.g., GRACE, TIMI)• Absence of high-risk features• High risk for catheterization-related
complications• Patient not a revascularization candidate
(with either PCI or CABG)• Patient prefers conservative therapy
GNL 2011
Right Coronary Artery
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Left Coronary System Left Coronary System
Long-term Rx: ACS
1. Aspirin 81 mg daily (lifelong)
2. Clopidogrel, Prasugrel or Ticagrelor (at least one year)
3. β-Blocker
4. Lipid-lowering agentgoal LDL < 70
5. ACEI or ARB especially for patients with CHF, LV dysfunction (EF<0.40), hypertension, or diabetes
6. Aldosterone blockers (Eplerenone) for patients with LV EF < 40% and CHF.
7. Smoke cessation and lifestyle modifications as indicated
Today’s Topics
Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD?
Case 2: When to look for and treat secondary hypertension due to renal artery disease?
Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis?
� Younger (<50), women, “beads on a string” angio� Progression to complete occlusion of renal artery rare� 80% Medial fibroplasia >> intimal (~10%) or
adventitial� 60% bilateral� In 25%, disease extends into segmental arteries� Other arteries can also be involved (carotid,
vertebral, iliac and mesenteric)� All patients need head imaging to r/o cerebral
aneurysms
Atherosclerotic Renal Artery Disease (RAS)– Prevalence of RAS ~1-6%– As high as 25-50% if atherosclerosis is present in other vascular beds
– 70-80% unilateral– Most common cause of secondary HTN– Probably, 10-15% of patients beginning dialysis have RAS of some severity
ACC/AHA Practice Guidelines 2005; White CJ 2007
Renal Artery Disease (RAS)– Progressive disease:
� 48% of patients with <60% stenosis progress to >60% over 3 years
� 39% patients with >75% stenosis progress to complete occlusion over 1-5 years
– Average progression ~7% per year– Note that progression of RAS and loss of renal function occur independently of blood pressure control
ACC/AHA Practice Guidelines 2005; White CJ 2007
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Clinical Clues to the Diagnosis of RAS
� Onset of HTN before age 30 or severe HTN after age 55� Accelerated, resistant, or malignant HTN� New azotemia or worsening renal fxn after Ace-inhibitor or ARB Rx� Unexplained atrophic kidney or size discrepancy between kidneys > 1.5 cm� Sudden unexplained pulmonary edema� Unexplained renal dysfunction� Multi-vessel CAD
ACC/AHA Practice Guidelines 2005; White CJ 2007
Asymptomatic RAS� No evidence to support benefit for treatment of asymptomatic RAS
� Class IIb (level of evidence C) �treatment of significant bilateral RAS or unilateral RAS in solitary kidney
Cardiac Destabilization Syndromes
� Class I (LOE B)– Revascularization is indicated in patients with hemodynamically significant RAS if recurrent unexplained heart failure or sudden unexplained pulmomary edema
� Class IIa (LOE B)– Revascularization is reasonable for unilateral
significant RAS with unstable anginaACC/AHA Practice Guidelines 2005
Conditions to At Least Consider Revascularization if RAS ≥ ~70% (Controversial)� Medically refractory hypertension (≥3 Rx at max doses) >140/90. But also consider if:
– Malignant HTN on meds: end-organ damage– Accelerated HTN: sudden, persistent worsening of previously controlled HTN
� Significant HTN + FMD� ARF after starting ACE-I� Recurrent flash pulmonary edema in setting of uncontrolled HTN� Severe RAS in solitary kidney� Severe bilateral RAS� Subacute renal failure (<6 mo), esp if creat <3.0, kidney size ≥ 9 cm in length
1. Calhoun DA, et al. Circulation. 2008;117;e510-e526.2. Makris A, et al. Int J Hypertens. 2011;doi: 10.4061/2011/598694.3. Papademetriou V, et al. Int J Hypertens. 2011;doi:10.4061/2011/196518.
Causes of PseudoresistantHypertension1,2
Suboptimal dosing of antihypertensive agents
White coat effect
Suboptimal BP measurement technique
Lifestyle factors
Medications that interfere with BP control
Pseudoresistance caused by poor adherence to prescribed medication
However, a majority of
patients with resistant
hypertension and no identifiable
secondary causes have an activated
sympathetic nervous system and increased sympathetic outflow3
Secondary Causes of Hypertension1,2
Obstructive sleep apnea
Primary aldosteronism
Renal artery stenosis
Caution: The Symplicity® Renal Denervation System™ is an Investigational Device. Limited by U.S. law to investigational use.
Even Small Reductions in BP Reduce Risk of CV Mortality
SBP = systolic blood pressure.Lewington S, et al. Lancet. 2002;360:1903-1913.
2 mm Hg decrease in mean office SBP 10% reduction in risk
of stroke mortality
7% reduction in risk of ischemic heart disease mortality
Caution: The Symplicity® Renal Denervation System™ is an Investigational Device. Limited by U.S. law to investigational use. Caution: The Symplicity® Catheter System™ is an Investigational Device. Limited by U.S. law to investigational
• The SNS supplies catabolic signals to the body, acting whenever rapid response to the environment is needed
• Functions include:
– Accelerating the heart
– Dilating coronary vessels
– Increasing arterial BP
– Emptying blood reservoirs
– Dilating bronchi
– Releasing glucose
– Inhibiting GI activityGI=gastrointestinal.Campbell WW. DeJong’s The Neurologic Examination: Incorporating the Fundamentals of Neuroanatomy and Neurophysiology. 6th ed. 2005.
Symplicity Investigational Catheter Device• Generator will automatically control RF energy delivery:
– Power automatically ramped and maintained (5-8W)– Continuously monitors temperature and impedance– Automatically shuts off after 2 min or when either impedance or
temperature exceed program limits
Flexible Tip (self-orienting)
5mm 12mmDeflectable
Shaft
EnligHTN – St. Jude Medical OneShot – CovidienSingle 2-minute inflation
Initial Cohort – Reported in the Lancet , 2009:-First-in-man, non-randomized-Cohort of 45 patients with resistant HTN (SBP ≥160 mmHg on ≥3 anti-HTN drugs, including a diuretic; eGFR ≥ 45 mL/min) - 12-month data\
Expanded Cohort – This Report (Symplicity HTN-1):-Expanded cohort of patients (n=153)-24-month follow-up
• Purpose: To demonstrate the effectiveness of catheter-based renal denervation for reducing blood pressure in patients with uncontrolled hypertension in a prospective, randomized, controlled, clinical trial
• Patients: 106 patients randomized 1:1 to treatment with renal denervation vs. control
• Clinical Sites: 24 centers in Europe, Australia, & New Zealand (67% were designated hypertension centers of excellence)
• Patient and Research staff assessing BP are blinded to treatment status
• No changes in medications for 6M
• Office SBP ? 160 mmHg• Full doses of ? 3 meds •
in past 2 wks• No plan to change meds
for 6 M
Initial Screening2 weeks
ConfirmatoryScreening
Renal Angiogram
Home BP & Med Confirmation
2 weeks
Home BP & Med Confirmation
2 weeks
1M 3M
3M1M
InitialScreening ABPM
Possible additional benefits of renal denervation
� Treatment of heart failure? � Improvements in glucose metabolism?
� Sympathetic hyperactivity– Shifts blood from striated skeletal muscle to visceral tissue– Visceral tissue is less insulin sensitive than striated muscle– Sympathetic activity increases glucagon secretion
� Inhibition of the sympathetic nervous system by moxonidine has been shown to improve glucose metabolism
� Reduces atrial fibrillation recurrence when combined with pulmonary vein isolation?
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Today’s Topics
Case 1: When to worry about a stress test result and how best to manage high risk patients with CAD?
Case 2: When to look for and treat secondary hypertension due to renal artery disease?
Case 3: What to do with non-operable or high-risk patients with severe aortic stenosis?
~1/3 of patients with severe symptomatic aortic stenosis patients do not undergo AVR
1. Bouma B J et al. To operate or not on elderly pat ients with aortic stenosis: the decision and its c onsequences. Heart 1999;82:143-1482. Iung B et al. A prospective survey of patients wi th valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. European Heart J ournal
2003;24:1231-1243 (*includes both Aortic Stenosis a nd Mitral Regurgitation patients)3. Pellikka, Sarano et al. Outcome of 622 Adults wit h Asymptomatic, Hemodynamically Significant Aortic Stenosis During Prolonged Follow-Up. Circulation 20 054. Charlson E et al. Decision-making and outcomes i n severe symptomatic aortic stenosis. J Heart Valv e Dis2006;15:312-321
Transfemoral Transapical
TAVRTransfemoral and Transapical Study Devices
Edwards SAPIEN THV23 and 26 mm valves
RetroFlex 22 and 24 F sheaths
Ascendra 24 and 26 F sheaths
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N = 699 N = 358High RiskHigh Risk InoperableInoperable
PARTNER Study Design
Symptomatic Severe Aortic Stenosis
ASSESSMENT: High-Risk AVR Candidate3,105 Total Patients Screened
ASSESSMENT: High-Risk AVR Candidate3,105 Total Patients Screened
Total = 1,057 patients
2 Parallel Trials: Individually Powered
StandardTherapy
ASSESSMENT: Transfemoral
Access
ASSESSMENT: Transfemoral
Access
Not In Study
TF TAVR
Primary Endpoint: All-Cause Mortality Over Length of Trial (Superiority)
Co-Primary Endpoint: Composite of All-Cause Mortali tyand Repeat Hospitalization (Superiority)
Note: Percents are of patients in the trial (n/179) .
Conclusions (1)
At 2 years, in patients with symptomatic severe AS who are not suitable candidates for surgery…
• TAVR remained superior to standard therapy with incremental benefit from 1 to 2 years, markedly reducing the rates of…
� All cause mortality
� Cardiovascular mortality
� Repeat hospitalization
• TAVR improved NYHA functional status and decreased Class III/IV symptoms compared to standard therapy (17% vs 64%; p < 0.001).
89
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Conclusions (2)
• There were more neurologic events in TAVR patients vs Standard Rx (16.2% vs 5.5%; p = 0.003) with 5 ne w events (3 strokes and 2 TIAs) between 1-2 years in TAVR patients.
90
N = 179
N = 358InoperableInoperable
StandardTherapy
ASSESSMENT: Transfemoral
Access
ASSESSMENT: Transfemoral
Access
Not In Study
TF TAVR
Primary Endpoint: All-Cause Mortality Over Length of Trial (Superiority)
Co-Primary Endpoint: Composite of All-Cause Mortali tyand Repeat Hospitalization (Superiority)
1:1 Randomization
VS
Yes No
N = 179
TF TAVR AVR
Primary Endpoint: All-Cause Mortality at 1 yr(Non-inferiority)
TA TAVR AVR
VSVS
N = 248 N = 104 N = 103N = 244
PARTNER Study Design
Symptomatic Severe Aortic Stenosis
ASSESSMENT: High-Risk AVR Candidate3,105 Total Patients Screened
ASSESSMENT: High-Risk AVR Candidate3,105 Total Patients Screened
Total = 1,057 patients
2 Parallel Trials: Individually Powered
N = 699 High RiskHigh Risk
ASSESSMENT: Transfemoral
Access
ASSESSMENT: Transfemoral
Access
Transapical (TA)Transfemoral (TF)
1:1 Randomization1:1 Randomization
Yes No
0
0.1
0.2
0.3
0.4
0.5
0 6 12 18 24
TAVR
AVR
Months
348 298 260 147 67
351 252 236 139 65
No. at Risk
TAVR
AVR
26.8
24.2
Primary Endpoint:All-Cause Mortality at 1 Year
HR [95% CI] =0.93 [0.71, 1.22]
P (log rank) = 0.62
All-Cause MortalityTransfemoral (N=492)
Months
244 215 188 119 59
248 180 168 109 56
No. at Risk
TAVR
AVR
26.4
22.2
HR [95% CI] =0.83 [0.60, 1.15]
P (log rank) = 0.25
0
0.1
0.2
0.3
0.4
0.5
0 6 12 18 24
TAVR
AVR
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104 83 72 28 8
103 72 68 30 9
29.0
27.9
TAVR
AVR
MonthsNo. at Risk
All-Cause MortalityTransapical (N=207)
HR [95% CI] =1.22 [0.75, 1.98]
P (log rank) = 0.41
0
0.1
0.2
0.3
0.4
0.5
0 6 12 18 24
TAVR
AVR
30 Days 1 Year
OutcomeTAVR
(N = 348)AVR
(N = 351)TAVR
(N = 348)AVR
(N = 351)
All Stroke or TIA – no. (%) 19 (5.5) 8 (2.4) 0.04 27 (8. 3) 13 (4.3) 0.04