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CLINICAL STUDY: HEART FAILURE

Antecedent hypertension and heart failure after myocardial infarction

A. Mark Richards, MD, PhD^,*, M. Gary Nicholls, MD, FACC^*, Richard W. Troughton, PhD^*, John G. Lainchbury, MD, John Elliott, MB, ChB, PhD, Christopher Frampton, PhD^*, Eric A. Espiner, MD^*, Ian G. Crozier, MD^*, Timothy G. Yandle, PhD^* and John Turner, MD

^* Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch Hospital, Christchurch, New Zealand
Cardiology, Christchurch Hospital, Christchurch, New Zealand
Nuclear Medicine, Christchurch Hospital, Christchurch, New Zealand

Manuscript received June 21, 2001; revised manuscript received January 3, 2002, accepted January 11, 2002.

^* Reprint requests and correspondence: Dr. A. Mark Richards, Department of Medicine, Christchurch Hospital, Riccarton Avenue, P O Box 4345, Christchurch, New Zealand.
barbara.griffin{at}chmeds.ac.nz

OBJECTIVES: We sought to assess the relationship of antecedent hypertension to neurohormones, ventricular remodeling and clinical heart failure (HF) after myocardial infarction (MI).

BACKGROUND: Heart failure is a probable contributor to the increased mortality observed after MI in those with antecedent hypertension. Hence, neurohormonal activation, adverse ventricular remodeling and a higher incidence of clinical HF may be expected in this group. However, no previous report has documented serial postinfarction neurohumoral status, serial left ventricular imaging and clinical outcomes over prolonged follow-up in a broad spectrum of patients with and without antecedent hypertension.

METHODS: Inpatient events were documented in 1,093 consecutive patients (436 hypertensive and 657 normotensive) with acute MI. In 68% (282 hypertensive, 465 normotensive) serial neurohormonal sampling and radionuclide ventriculography were performed one to four days and three to five months after infarction. Clinical outcomes were recorded over a mean follow-up of two years.

RESULTS: Plasma neurohormones were significantly higher in hypertensives than in normotensives one to four days and three to five months after infarction. From similar initial values, left ventricular volumes increased significantly in hypertensives, compared with normotensives. Left ventricular ejection fraction rose significantly in normotensive but not hypertensive patients. Together with higher inpatient (8.1% vs. 4.4%, p < 0.002) and post-discharge mortality (9.5% vs. 5.5%, p = 0.043), hypertensive patients incurred more inpatient HF (33% vs. 24%, p < 0.001) and more late HF requiring readmission to hospital (12.4% vs. 5.5%, p < 0.001). Antecedent hypertension predicted late HF in patients >64 years of age with neurohormonal activation and early left ventricular dilation.

CONCLUSIONS: Antecedent hypertension interacts with age, neurohumoral activation and early ventricular remodeling to confer greater risk of HF after MI.

Abbreviations and Acronyms   ACE   angiotensin-converting enzyme   ADM   adrenomedullin   ANP   atrial natriuretic peptide   BNP   brain natriuretic peptide   cGMP   cyclic guanosine monophosphate   CK   creatine kinase   ECG   electrocardiogram   ET-1   endothelin 1   HF   heart failure   MI   myocardial infarction   N-ANP   aminoterminal atrial natriuretic peptide   N-BNP   aminoterminal brain natriuretic peptide

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