Hypertension and Heart Failure Sine Heart Failure

Can you imagine a young asymptomatic patient with a blood pressure of 141/91 mm Hg being told that he/she has stage A heart failure? The recent American College of Cardiology/American Heart Association (ACC/AHA) Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult have introduced the concept that clinicians should diagnose heart failure sine heart failure (Table). ¹ The intentions of these guidelines are good, i.e., to cause clinicians to treat diseases that may result in heart failure. However, unless corrected, this concept is destined to cause confusion among the rank and file of physicians caring for patients with heart disease. The manifestations of misuse of terms may be seen in basic research, applied research—including clinical trials, and treatment of individual patients.

Table.

ACC/AHA Guidelines for the Diagnosis and Management of Heart Failure (HF)

Stage	Description	Examples
A	Patients at high risk of developing HF because of the presence of conditions that are strongly associated with the development of HF. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF.	Systemic hypertension, coronary artery disease, diabetes mellitus, history of cardiotoxic drug therapy or alcohol abuse, personal history of rheumatic fever, family history of cardiomyopathy
B	Patients who have developed structural heart disease that is strongly associated with the development of HF but who have never shown signs or symptoms of HF.	Left ventricular hypertrophy or fibrosis, left ventricular dilatation or hypocontractility, asymptomatic valvular heart disease, previous myocardial infarction
From the American College of Cardiology/American Heart Association (ACC/AHA) Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. Available at: http:www.acc.orgclinicalguidelinesfailuretable1.htm 1

Hypertension and heart failure are both major public health problems in the United States; 43 million (24%) of the adult population have hypertension, and hypertension is the most important modifiable risk factor for heart failure. ² , ³ The incidence of heart failure has been increasing steadily in the United States during the past two decades; hypertension carried a relative risk of 1.22 (95% confidence interval, 1.04–1.42) as an independent risk factor. ³ Heart failure is a major cause of chronic disability, and annual expenditures for the approximately 3 million persons who have heart failure currently exceed $10 billion.

Heart failure is, of course, a clinical entity that has received increasing, and deserved, attention as the incidence and prevalence of the syndrome has risen with the associated burden of morbidity and mortality and drain on economic resources. A great deal of money and effort has been expended in educating clinicians to recognize and treat heart failure. A conceptual difficulty arises for clinicians when they are now urged to ignore what they have been taught and to recognize “heart failure” before the development of signs and symptoms.

Heart failure often is perceived as a “disease” when, in fact, it is a clinical syndrome rooted in physiologic derangements. The “disease” concept of heart failure is advanced by the finding that final common pathways exist for progression and deterioration with advancement to end‐stage heart failure or sudden cardiac death. The “hemodynamic” or “neurohormonal” hypotheses concerning these pathways have dominated our thinking about heart failure; devising therapeutic strategies based on these hypotheses have, nevertheless, yielded dividends. If, however, we wish to prevent this late clinical stage of cardiac dysfunction, the focus of attention must shift to earlier stages of specific etiologies of heart failure, i.e., cardiomyopathies. Cardiomyopathy may exist in a hypertensive patient long before the presence of heart failure. Labeling a patient as stage A heart failure, in the absence of heart failure, may be a mistake.

Cardiomyopathy, the disease of heart muscle, is the critical “C” in “CHF,” and underlies virtually all of the cases of chronic heart failure. Heart failure is only one outcome of cardiomyopathy, and, unlike the term “heart failure,” cardiomyopathy can exist in a preclinical, subclinical, or latent state. Moreover, the diagnosis of cardiomyopathy cries out for the clinician to consider specific etiologic factors, many that are reversible. Increasingly, pluricausal cardiomyopathies, i.e., due to more than one etiology, are common. The present time is particularly opportune for an increased emphasis on cardiomyopathy as research has identified numerous genetic causes and more is understood regarding the pathophysiology associated with cardiac remodeling in general. It will become increasingly important for clinical research to distinguish between the clinical phenotypes of heart failure and the many phenotypes of the cardiomyopathies. Future clinical trials will assuredly focus on genetic/environmental interactions in an effort to find the “right therapy for the right patients.”

Reorientation of clinicians to think of cardiomyopathy (with or without heart failure; C±HF) instead of congestive heart failure (CHF) will not be easy. The foundation for this difficulty has been laid by the inconsistent way in which the term “cardiomyopathy” has been defined and classified for the clinician. This process began in 1968 when the World Health Organization suggested that the term “idiopathic cardiomegaly” be used for cardiomyopathies. ⁴ The use of the term “idiopathic” as a specific etiologic entity is puzzling. The 1980 recommendations of the World Health Organization (WHO) and International Society and Federation of Cardiology (ISFC), which included the designation of diseases of heart muscle of unknown cause as “cardiomyopathy,” and all others as “specific heart muscle diseases,” ⁵ added to the perception of “idiopathic” as a specific entity.

The latest WHO/ISFC classification has at least eliminated the idea of “idiopathic” as a specific etiologic entity. ⁶ Now, there is no category in which to place cardiomyopathies for which no cause can be found; cardiomyopathy, not otherwise specified, is standard for other organ disease classifications. Worse, the current WHO/ISFC classification requires the demonstration of cardiac dysfunction before the term cardiomyopathy may be applied. This requirement would prevent the recognition and detection of subclinical cardiomyopathy, as in some patients with hypertension, and thwart attempts to prevent disease progression at an early stage. Finally, despite exciting research findings into a genetic basis for many cardiomyopathies, the WHO/ISCF classification has no category into which they may be placed.

Thus, the individual with a cardiovascular derangement that may produce an increase in systemic arterial blood pressure above the optimal level, i.e., higher than necessary to provide adequate perfusion of vascular beds, has potential, or latent, hypertensive cardiomyopathy. As cardiac remodeling occurs, the cardiomyopathy may be detectable without symptoms, i.e., subclinical cardiomyopathy. Finally, when signs and symptoms associated with cardiac dysfunction occur, the condition is hypertensive cardiomyopathy with heart failure; the left ventricular ejection fraction may, or may not, be decreased.

Clinicians who treat patients with hypertension are aware of the significance of hypertension in the development of heart failure. They may be called uponto restore appropriate nomenclature to various stages in the evolution of hypertensive cardiomyopathy to enable clinicians to better prevent this dire consequence of hypertension. A revision of the concept endorsed by the ACC/AHA guidelines will permit the patient with early hypertensive cardiomyopathy to be treated without being told that he or she has a nonexistent condition, i.e., heart failure.