This study will test the hypothesis that increases in ventricular-vascular stiffness can be demonstrated by arterial tonometry and echocardiography in subjects with heart failure with preserved ejection fraction (HF-nlEF)(i.e. normal left ventricular function.) We will also track changes in pulsatile hemodynamics over time in subjects hospitalized with HF-nlEF.

The pathophysiologic mechanisms responsible for the development of heart failure in people with preserved ejection fraction (i.e. normal left ventricular function) remain poorly understood. One possible mechanism may be the contribution of increased arterial stiffness to changes in pulsatile hemodynamic load during ventricular systole, implicating abnormal ventricular-vascular interactions throughout the cardiac cycle in the pathogenesis of heart failure with normal ejection fraction.

To investigate changes in ventricular-vascular stiffness in subjects with heart failure and normal left ventricular function, comparisons will be made between 3 distinct sub-populations:

• subjects with heart failure and normal ejection fraction
• non-diabetic hypertensive controls
• normotensive controls

Inclusion Criteria:

Subjects with heart failure and preserved ejection fraction

• clinical signs of heart failure
• serum brain natriuretic peptide (BNP) >100pg/mL
• NYHA functional class II-IV
• left ventricular ejection fraction(LVEF) >=50% measured by echocardiography
• Non-diabetic subjects with hypertension
• treated or untreated essential hypertension
• LVEF >=50% measured by echocardiography

Diabetic subjects with hypertension

• Type 2 diabetes
• treated or untreated essential hypertension
• LVEF >=50% measured by echocardiography

Normotensive control subjects

• normal blood pressure (i.e. < 140/90 mmHg)
• LVEF >=50% measured by echocardiography

Exclusion Criteria:

Subjects with heart failure and preserved ejection fraction

• atrial fibrillation
• symptoms of angina or a myocardial infarction (MI) within 6 months
• known significant coronary artery disease (CAD) (stenosis > 70%)
• significant valvular heart disease
• restrictive/constrictive heart disease
• inability to lie flat for procedure (estimated duration 1 hour)

Non-diabetic subjects with hypertension

• atrial fibrillation
• symptoms of angina or a myocardial infarction (MI) within 6 months
• known significant coronary artery disease (CAD) (stenosis > 70%)
• significant valvular heart disease
• restrictive/constrictive heart disease
• inability to lie flat for procedure (estimated duration 1 hour)
• prior history of heart failure or unexplained dyspnea

Diabetic subjects with hypertension

• atrial fibrillation
• symptoms of angina or a myocardial infarction (MI) within 6 months
• known significant coronary artery disease (CAD) (stenosis > 70%)
• significant valvular heart disease
• restrictive/constrictive heart disease
• inability to lie flat for procedure (estimated duration 1 hour)
• prior history of heart failure or unexplained dyspnea

Normotensive control subjects

• prior history of structural heart disease or ventricular hypertrophy
• treatment with HMG-Co(A)reductase inhibitors (statins)
• anti-hypertensive medications
• cigarette smoking
• cocaine use
• excessive alcohol intake

adults with heart failure and preserved left ventricular function