CRS-I-Treatment

Alan

Maisel

MD

Professor of

Medicine,

University of

California,

San Diego

Director

Coronary Care

Unit And Heart

Failure Program

San Diego

Veterans

Hospital

Outcomes in Patients Hospitalized

With HF

N = 38,702Aghababian RV. Rev Cardiovasc Med. 2002;3(suppl 4):S3

Jong P et al. Arch Intern Med. 2002;162:1689

0

25

50

75

100

20%

50%

30Days

6Months

Hospital Readmissions

0

25

50

75

100

12%

50%

30Days

12Months

Mortality

33%

5Years

Median LOS: 6 days

• Until recently we

didn’t really have

any effective, non-

toxic treatments for

CHF

Treatment of Acute HF

Diuretics

Fluid

volume

Vasodilators

Preload

and/or

afterload

Inotropes

Contrac

-

tility

Natriuretic

Peptides

Fluid volume

Preload

Afterload

Neuro-

hormes

Increase

lusitropy

Profiles and Therapies of Advanced Heart Failure

Yes

R. Bourge, UAB Cardiology (adapted from L. Stevenson)

Stevenson LW. Eur J Heart Failure 1999;1:251-257

No

Warm and Dry

PCW and CI

normal

Warm and Wet

PCW elevated

CI normal

Cold and Wet

PCW elevated

CI decreased

Cold and Dry

PCW low/normal

CI decreased

Vasodilators

Nitroprusside

Nitroglycerine

Nesiritide

Inotropic Drugs

Dobutamine

Milrinone

Calcium Sensitizers

Nl SVR High SVR

Congestion at Rest

Low

Perfusion

at Rest

No

Yes

Complications of Diuretic Therapy

for Heart Failure

Na = sodium; Mg = magnesium; GFR = glomerular filtration rate; PRA = plasma renin activity.Kaplan NM., Treatment of Hypertension: Drug Therapy in Clinical Hypertension (p. 203) in Clinical Hypertension, 6th. Ed. Baltimore: William and Wilkins 1994.

Distal Ca++Reabsorption

Plasma Volume

Uric AcidClearance

HypomagnesemiaDiuretic Therapy

Cardiac Output

Renal Reabsorption of Na (and Mg)

Renal Blood Flow

Hyponatremia

PRA

GFR

ProximalReabsorption

Aldosterone

Kaliuresis

Hypokalemia

Glucose IntoleranceHypocalcemiaHyperuricemia

CalciumClearance

Pre-renalAzotemia

Neurohumoral Activation

The Natriuretic Peptide System is Overwhelmed in Acute Decompensated Heart Failure

Adapted from Burnett JC, J Hypertens 1999;17(Suppl 1):S37-S43

Angiotensin II

Epinephrine

Endothelin

ANP BNP

Aldosterone

Human B-type Natriuretic

Peptide (hBNP)

Nesiritide is identical

to endogenous hBNP

Mechanism of Action:

via receptor binding

to GC-A receptor and

cGMP production (no

impact on cAMP)

rhBNPD

R I

M

K

R

G

SS

S

S

G

L

GF

CC

S S

GSGQVM

K V LR

RH

KPS

Effects of NesiritideVenous, arterial, coronary

VASODILATION

CARDIAC

INDEX

Preload

Afterload

PCWP

Dyspnea

HEMODYNAMIC

CARDIAC

No increase in HR

Not proarrhythmic

Aldosterone

Endothelin

Norepinephrine

SYMPATHETIC AND

NEUROHORMONAL SYSTEMS

NATRIURESIS

DIURESIS

Fluid volume

Preload

Diuretic

usage

RENAL

VMAC – Clinical Benefit• VMAC demonstrated that NATRECOR® with

standard therapy is superior in improving dyspnea and reducing filling pressure compared to placebo with standard therapy

• “Standard care” medications during study drug included any of the following:– IV diuretics (73%)

– non-IV diuretics (48%)

– oral ACE inhibitors (58%)

– aspirin (45%)

– oral, topical, or sublingual

nitrates (34%)

– beta-blockers (27%)

– warfarin (15%)

– statins (26%)

– class III antiarrhythmics

(16%)

– A-II receptor antagonists

(8%)

– hydralazine (9%)

– dobutamine (23%)

– dopamine (6%)Reference: NATRECOR® Full Prescribing Information.

Data on file, Scios Inc.

Hemodynamic Effects of Nesiritide

vs Placebo vs IV NTG

*†

*

†

*

†

††

†

†

*

During 3-hr placebo period

Placebo n = 62

IV NTG n = 60

Nesiritide n = 124

After 3-hr period

IV NTG n = 92

Nesiritide n = 154

Publication Committee for the VMAC Investigators. JAMA. 2002;287:1531

*P0.05 vs placebo†P0.05 vs IV NTG

PCWP – Placebo

PCWP – IV NTG

PCWP – Nesiritide

End of Placebo-Controlled Period

Time on Study Drug (hr)

0 0.25 0.5 1 2 3 6 9 12 24 36 48

–9

–8

–7

–6

–5

–4

–3

–2

–1

0

†

*

*

Ch

an

ge F

rom

Baselin

e i

n

PC

WP

(m

m H

g)

Nitroglycerin Dose and Change in

PCWP During Treatment With

Nitroglycerin

n = 9 (3 hr); n = 12 (>3 hr)

Added to standard therapy

Elkayam U et al. Am J Cardiol. 2004;93:237

0

20

40

60

80

100

120

140

160

180

0 3 6 9 12 15 18 21 24

Time (hr)

Nit

rog

lyceri

n D

ose (

mcg

/min

)

8

7

6

5

4

3

2

1

0

Ch

an

ge in

PC

WP

(mm

Hg

)

NTG dose

Change in PCWP

*

*

*

*

*

*

* P<0.05 vs baseline

Nesiritide Versus Other Vasodilators

Parameters Nitroglycerin NitroprussideNesiritide

Tachyphylaxis Yes No No

Toxic Metabolites No Yes No

Hypotension Yes Yes Yes

Special handling Glass Light No

Headache Yes Yes Yes

Action on RAAS ? Renin Aldosterone

Difficult titration No Yes No

Limitations of Current Therapies for Acute HF: Positive Inotropes

• Increased mortality1-3

– Milrinone

– Enoximone

– Imazodan

– Vesnarinone

– Dobutamine

– Xamoterol

– Ibopamine

• Increased risk of hospitalization

• Aggravation and induction of

arrhythmias (need telemetry)4

– Milrinone

– Dobutamine

– Dopamine

• Tachycardia

• Tachyphylaxis (dobutamine)

• Neurohormonal activation and/or

lack of suppression

• Physiologic effects antagonized

by -blockade (dobutamine,

dopamine)1Packer M et al. N Engl J Med. 1991;325:14682Cohn JN et al. N Engl J Med. 1998;339:18103The Xamoterol in Severe Heart Failure Study Group. Lancet. 1990;336:1 4Ewy GA. J Am Coll Cardiol. 1999;33:572

J Sackner-Bernstein,

M Kowalski, M Fox.

JAMA. 293 (15)

1900-5,

April 20, 2005

Acute Decompensated Heart Failure:

Nesiritide and Mortality

• No short-term therapy for ADHF has been proven to improve short- or long-term mortality rates.

• Nesiritide is the only approved ADHF therapy which has been shown in large, randomized trials to provide both significant symptomatic and hemodynamic improvement when added to standard care.

• Nesiritide has not been studied in a trial powered to evaluate an effect on mortality.

– 30-day mortality data available for 7 trials

– 6-month mortality data available for 4 trials

J Sackner-Bernstein, M Kowalski, M Fox.

JAMA. 293 (15) 1900-5, April 20, 2005

30-Day Mortality Hazard Ratios

VMAC

PROACTION

FUSION I

PRECEDENT

Efficacy

Comparative

Mills et al.

Note: Arrows depict studies included in JAMA publication

• A prospective, multi-center, randomized, double-blind, pilot study

– Included 279 randomized and treated heart failure patients undergoing

cardiac surgery with or without mitral valve repair/replacement

• NAPA was a Phase II, exploratory study

– No pre-specified primary endpoints; however there were pre-specified

areas of interest

– Not the labeled dose (no bolus)

– Limitations with this analysis

• 180-day mortality endpoint was added late in the study; as a result subjects

were lost to follow-up (3%), declined consent (9%) or did not respond to request

for information (13%), other* (6%) at 180 days.

• This study is too small to draw definitive mortality conclusions

– This study is not designed to demonstrate safety and effectiveness for this

use

• More robust trials are planned

NAPA TrialNesiritide Administered Peri-Anesthesia in Patients Undergoing

Cardiac Surgery

* Documented alive at days 174 to 179.

Nesiritide

(n=141)

% (n)

Placebo

(n=138)

% (n)

Hazard

Ratio

(95% CI)

P value

Kaplan-Meier rate

within 30 days

2.8%

(4/141)

5.9%

(8/138)

0.48

(0.14, 1.59)0.219

Kaplan-Meier rate

within 180 days

6.7%

(8/141)

14.7%

(17/138)

0.44

(0.19, 1.01)0.046

• 30-day mortality data were available for 132 patients

in the nesiritide group and 127 in the placebo

group.

• 180-day mortality data were available for 94 patients

treated with nesiritide and 95 patients treated with

placebo.

Reference: Luber JM, Jr., on behalf of the NAPA Investigators. J Card Fail. 2006; 12(6, suppl 1):S73-S74. Abstract 235. Scios will

submit a final report to FDA once its own internal validation of the data is complete.

NAPA Trial

30-Day and 180-Day Mortality

Reference: Luber JM, Jr., on behalf of the NAPA Investigators. J Card Fail. 2006; 12(6, suppl 1):S73-S74. Abstract 235. Scios will

submit a final report to FDA once its own internal validation of the data is complete.

In seven NATRECOR® clinical trials, through 30 days, 5.3% in the NATRECOR® treatment group died as compared with 4.3% in the

group treated with other standard medications. In four clinical trials, through 180 days, 21.7% in the NATRECOR® treatment group died as

compared with 21.5% in the group treated with other medications. There is not enough information to know about the effect of

NATRECOR® on mortality.

NAPA Trial

Kaplan-Meier Survival Curve by Treatment Goup

J Sackner-Bernstein,

HA Skopick,

KD Aronson.

Circ. 111 1487-91,

2005

Methods/Results

• 5 studies, N = 1,269

• Dose ranging from 0.01 to 0.06 g/kg/min

• “Even low-dose nesiritide (0.015 g/kg/min) significantly increased risk (p=0.012 and p=0.006 compared with non-inotrope and inotrope based controls, respectively)”

J Sackner-Bernstein, HA Skopick,

KD Aronson. Circ. 111 1487-91, 2005

SCr Increases with Nesiritide: Renal

Outcomes

• Prescribing Information, Precautions: Renal Effects

– “When NATRECOR® was initiated at doses higher than 0.01

mcg/kg/min (0.015 and 0.03 mcg/kg/min), there was an increased

rate of elevated SCr compared with standard therapies, although

the rate of acute renal failure and the need for dialysis was not

increased.”

– “In the 30-day follow-up period in VMAC, 5 patients in the NTG

group (2%) and 9 patients in the NATRECOR® group (3%) required

first-time dialysis.” (p=0.418)

Reference: NATRECOR® Full Prescribing Information.

NAPA TrialMean Change in Serum Creatinine (SCr) and Calculated Glomerular

Filtration Rate (cGFR) by Treatment Group and Baseline Renal Function

PARAMETERS OF INTEREST NESIRITIDE PLACEBO P

Peak SCr Increase (mg/dL)*

All Patients (n=266) 0.15 0.34 <0.001

Patients with baseline SCr >1.2 (n=62) 0.02 0.48 0.001

Maximum Decrease in cGFR (ml/min)*

All Patients (n=266) -10.8 -17.2 0.001

Patients with baseline SCr >1.2 (n=62) -0.2 -9.1 0.003

Postoperative SCr Increase >0.5 mg/dL*

All Patients (n=271) 7% 23% <0.001

Postoperative Urine Output (first 24 hrs.) (ml)

All Patients (n=271) 2926 2350 <0.001* Through discharge or hospital day 14, whichever came first

Reference: Hebeler RF Jr. on behalf of the NAPA investigators. Circulation May 30, 2006. Abstract 292

NATRECOR® may affect renal function in susceptible individuals. In patients with severe heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with NATRECOR® may be associated with azotemia. In the VMAC trial, through day 30, the incidence of elevations in creatinine to >0.5 mg/dL above baseline was 28% and 21% in the NATRECOR® and nitroglycerin groups, respectively. When NATRECOR® was initiated at doses higher than 0.01 mcg/kg/min, there was an increased rate of elevated serum creatinine over baseline compared with standard therapies, although the rate of acute renal failure and need for dialysis were not increased.

NAPA Trial

Mean Change from Baseline in Post-Op SCr

NATRECOR® may affect renal function in susceptible individuals. In patients with severe heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with NATRECOR® may be associated with azotemia. In the VMAC trial, through day 30, the incidence of elevations in creatinine to >0.5 mg/dL above baseline was 28% and 21% in the NATRECOR® and nitroglycerin groups, respectively. When NATRECOR® was initiated at doses higher than 0.01 mcg/kg/min, there was an increased rate of elevated serum creatinine over baseline compared with standard therapies, although the rate of acute renal failure and need for dialysis were not increased.

Reference: Luber JM, Jr., on behalf of the NAPA Investigators. J Card Fail. 2006; 12(6, suppl 1):S73-S74. Abstract 235. Scios will

submit a final report to FDA once its own internal validation of the data is complete.

Ideal Agent for Acute HF

• Vasodilator (venous and arterial)

• Rapidly decreases ventricular filling pressures

• Rapidly decreases symptoms of congestion

• Does not increase heart rate or directly increase contractility (decreases myocardial oxygen demand)

• Not proarrhythmic

• No tolerance

• Provides neurohormonal suppression

• Promotes diuresis/natriuresis

• Conveniently dosed (with or without PA catheterization)

• Minimal titration needed

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7

Braunwald Panel

Recommendations

• Nesiritide is approved for inpatient management of acute HF

• Use of nesiritide should be limited to patients presenting to the hospital with acute HF who have dyspnea at rest

• Physicians considering the use of nesiritide should consider

– Its efficacy in reducing dyspnea

– Possible risks of the drug

– Availability of alternate therapies to relieve HF symptoms

Scios Inc. press release. June 13, 2005. Available at: http://www.sciosinc.com/scios/pr_1118721302.

Accessed July 13, 2005

ADHERE CART: Predictors of Mortality

SYS BP 115n = 24,933

SYS BP 115n = 7150

6.41%

n = 5102

15.28%

n = 2048

21.94%

n = 62012.42%

n = 1425

5.49%

n = 4099

2.14%

n = 20,834

BUN 43N = 33,046

Greater thanLess than

2.68%

n = 25,122

8.98%

n = 7202

Cr 2.752045

Highest to Lowest Risk Cohort

OR 12.9 (95% CI 10.4-15.9)

Fonarow GC et al. JAMA 2005. 293:572

In-Hospital Mortality Risk by Initial

BNP Levels Reduced vs. Preserved

Systolic Function HF

48,629 (63%) out of 77,467 pt episodes had BNP assessment at initial evaluation

19,544 patients with LVEF < 0.40 and 18,164 patients with LVEF > 0.40

Q2 2003 to Q4 2004

1.4

2.8

3.8

6.4

0

1

2

3

4

5

6

7

InH

os

pit

al M

ort

ality

Q1 (<622) Q2 (622-1210) Q3 (1210-2310)

Q4 (>2310)

P<0.0001

1.5

2.7 2.8

5

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

5

InH

os

pit

al M

ort

ali

ty

Q1 (<336) Q2 (336-630) Q3 (630-1230) Q4 (>1230)

P<0.0001

LVEF < 0.40 LVEF > 0.40

Patient Outcomes by Quartiles of

BNP Levels in the ADHERE

Registry

48,629 (63%) out of 77,467 pt episodes had BNP assessment at initial evaluation.

Q2 2003 to Q4 2004

Q1

(<430)

Q2

(430-839)

Q3

(840-

1730)

Q4

(>1730)

P Value

Ventilation 3.1 3.7 3.9 4.1 P=0.0002

CPR 0.6 0.9 1.2 1.7 P<0.0001

Ultrafiltrat 0.6 0.8 1.6 5.0 P<0.0001

LOS (days) 5.2 5.7 5.9 6.3 P<0.0001

ICU admit

%

12.8 15.4 16.6 19.6 P<0.0001

ASx at DC 48.8 49.6 48.0 43.6 P<0.0001

High risk patient:• No change or increase in BNP level• Inadequate diuresis (<500cc)• Worsening renal function

SBP ≥ 90Nesiritide 1-2 days

IV Diuretics

SBP < 90InotropesPressors

+/- Swan Ganz Catheter

BNP level 6h after Nesiritide cessationthen re-check BNP

Improvement in symptoms/ BNP

Oral vasodilators and diuretics until euvolemic.D/C BNP level

Yes No

Consider• Angiography• IABP• Transplant• LVAD

Nesiritide 1-2 days, then po Vasodilators,diuretics

Low Risk Patient:• BNP level decreased• Adequate diuresis (500-1000cc)• No deterioration in renal function

Continue diuretics/vasodilators until euvolemic

BNP < 400Discharge

BNP ≥ 400Re-evaluate

Volume status

Discharge withearly follow-up

Nesiritide plus

diuretics

Euvolemic

Yes No

ALGORITHM FOR USE IN BNP TESTING IN PATIENTS WITH CHF

Yes

IV diuretic for 6 to 12 hoursNo

Initial BNP > 600&

Initial BUN > 40

Draw BNP, BUN

Write orders carefully

Continuous Aortic Flow

AugmentationOrqis® Cancion®

Ax – Fem graft

Cath : Fem:Fem

single Fem

• a – inflow (fem artery)

• b – pump

• c – pump motor

• d – controller

• e – flow sensor

• f – outflow (desc

a

b

c

d

e

f

Mechanism of Action

Continuous Aortic Flow Augmentation

Ventricular

UnloadingVasodilation Renal Effects

DiuresisHemodynamic improvement

Clinical Benefit

Nitric Oxide

Other mediators

Effects of CAFA on

Renal Function

Serum Creat n=20

1.0

1.1

1.2

1.3

1.4

1.5

BASELINE DAY 1 DAY 2 DAY 3

mg

%

p=0.02

Mechanical Therapy

Smaller devices

Less infection?

Opportunity

for explant

REMATCH Trial: All Cause Mortality

LV Assist

Device (n=68)

Control

(n=61)

P=0.001

6 12 18 240

100

80

60

40

20

0

30

Months

% E

ve

nt

Fre

e S

urv

iva

l

RR 0.52 (0.34,0.78)N Engl J Med 2001; 345: 1435

Limitations of Current LVAD Therapy

• Very expensive.

• Major commitment on the part of

physicians, nurses and hospitals for

continuing care.

• Small increase in survival rates after 2

years.

• Substantial risk of bleeding, infection and

device malfunction requiring in-hospital

care.

Limitations of Current LVAD Therapy

• Very expensive.

• Major commitment on the part of

physicians, nurses and hospitals for

continuing care.

• Small increase in survival rates after 2

years.

• Substantial risk of bleeding, infection and

device malfunction requiring in-hospital

care.

Donor Myocytes

Dilated CMP

Post LVAD

Mechanical Unloading Reverses The

Heart Failure Phenotype

Cell Transplantation For Treating

HF

• neonatal/adult CM

• embryonic stem cell

• bone marrow stem cell

• skeletal myoblast

• others

GM fibroblast

cardiac stem cells

Possible Graft

End

stage

heart

failureNew Myocytes

Functional recovery

of diseased hearts

Undefined mechanisms

animals, human

BOOST Results

Wollert KC et al. Lancet, July 2004

Titrating therapy by Natriuretic

peptide levels

• NP levels above baseline

usually mean volume

overload

• NP levels can help one

achieve euvolemia and

monitor treatment

• NP levels can help

determine appropriate

discharge from the hospital

Changes in BNP and PAW* Levels

During 24 Hours of Treatment

Msaisel, A. et al. J Cardiac Failure, Vol. 7, No. 1, 2001

N = 15 (responders)

PA

W (

mm

Hg

)

Hours

BN

P (p

g/m

l)

15

17

19

21

23

25

27

29

31

33

baseline 4 8 12 16 20 24600

700

800

900

1000

1100

1200

1300

PAWBNP

*Pulmonary artery wedge.

250500

800

1750

500

1000

1500

2000

2500

I II III IV

Dry ( NYHA Euvolemic state)

In volume overloaded patients: BNP level = baseline BNP(dry)

plus change due to increased volume(wet)B

NP

lev

el (

pg/m

l)

NYHA Class - Euvolemic (Dry) BNP

Wet (Change due to volume overload)

28

17

14

6

3

kDaRec. A B C D E blank Rec.

Clinical BNP Results pg/ mL: A B C D E

Maisel 3920 3720 4010 2090 127

in-house Triage 1140 1440 1260 1570 584

Major form of BNP in patients with CHF is proBNP

proBNP

BNP

5 CHF patients:

Liang, Maisel et al., JACC 2007

Serial BNP for Guiding Treatment

During Hospitalization?

Courtesy of Damien Logeart.

BNP:

It’s About Improving Patient Care

Logeart et al. Predischarge BNP Assay for Identifying Patients at High Risk of

Re-Admission After Decompensated Heart Failure. JACC 43(4): 635-41

Logeart D. et al. J Am Coll Cardiol. 2004 Feb 18;43(4):635-41

Follow-up (days)

Hazard ratios

of 2nd and 3rd

versus 1st BNP range

Death

or

readm

issio

n (

%)

100

75

50

25

0

0 30 60 90 120 150 180

Predischarge BNP >700ng/l

n =41, events =38

Predischarge BNP 350 - 700ng/l

n =50, events =30

Predischarge BNP <350ng/l

n =111, events =18

p <0.0001

p <0.0001

15.2

5.1

1

Bringing BNP Into the Clinic —or Bringing the Clinic to BNP

Needs to be interpreted in context

• Does not take the place of history, physical exam

• To interpret value must have understanding of BNP and heart failure syndrome

• Must have previous BNP values to which to refer

BN

P (

pg/m

l)

262248

1180

1050

275

0

200

400

600

800

1000

1200

1400

A B C D E

A. Decompensated CHF (IV)

B. After treatment (II)

C. Clinic - 2 months later (II)

D. Stopped Meds - 3 months later (IV)

E. After treatment (II)

Algorithms for BNP Outpatient ManagementTELEMEDICINE

Algorithms for BNP Outpatient ManagementOUTPATIENT CLINC

The Holy Grail

• Can BNP levels be

used to titrate

outpatient therapy?

Targets in Treatment

• In many conditions treatment

can be titrated against a

target :

Hypertension Blood Pressure

Diabetes glucose, HbA1c

Lipids Cholesterol

Heart Failure Treatment Targets

There is currently

no target for treatment

of heart failure that is:

– Objective

– Reliable

– Practical

– Inexpensive

Neurohormones in Heart Failure

• Neurohumoral activation

– Marker of severity and prognosis in CHF

• BNP levels

– Reflect LV wall stress/ filling pressure

– Correlate with LV ejection fraction

– Indicate prognosis in CHF and after MI

– Fall with effective ACEI / diuretic therapy

Benefit of BNP plasma levels for optimising

therapy in patients with systolic heart failure :

The Systolic hearT fAilure tReatment Supported

by BNP trial (STARS-BNP) multicenter

randomised study.

For STARS-BNP Investigators on behalf of the working group on Heart failure of the

French Society of Cardiology

STARS

BNP

BNP group Clinical group p

all causes hospitalizations N: 52 60 NS

Hospitalizations related to HF N 22 48 P<0,001

Death all causes N: 7 11 NS

Death related to HF N: 3 9 P<0,05

HF related death and hospitalizations N: 25 57 P<0,001

End Points

STARS

BNP

Patient

Doctor

Our patients

really love

the BNP test!

And

they

live

longer!

People

feel

better

when

their

BNP

levels

are

lower

Patient

compliance

often improves

when patients

also have an

objective way

to monitor their

condition

BNP on Every Street Corner?

Some

would

like

Nothing

better

than

To burst

the

bubble

BNP and Guidelines

• As with every new diagnostic

or treatment modality,

guidelines often lag behind

state-of-the-art practice

• It is very encouraging to see

that after only several years

of introduction into clinical

practice, the use of BNP

is already recommended

by all major guidelines

Suspected Acute Heart

Failure

Assess Symptoms and

SignsHeart Disease?

ECG / BNP/ X-

ray?

Nor

mal

Evaluate function

byEchocardiography / other

imaging

Nor

mal

Abnorm

al

Abnorm

alHeart Failure, assess

by

Echocardiography Selected tests(angio, hemodynamic

monitoring, PAC)Characterize type and

severity

Consider other diagnosis

European Heart J. 2005;26:385-6.NEED MORE

COMPLETE CITATION

Diagnostic Tests Alone Will Not

Accomplish Our Goals…

Being an MD at a distanceAirport get phone calls

foot ball game

Or just relaxing

What’s his

BNP ?

We Need to Be Good Clinicians

at the Bedside First!

Modern

technology

is not always

available

to us

It takes longer

to use history,

physical exam

skills AND

technology…

Thank You!