Heart failure may be recognized as a clinical end-point in nearly all cardiac diseases. Because the underlying cause of the development of heart failure varies significantly between species and disease conditions, it is often difficult to define heart failure accurately and concisely. In 1994, a panel of the National Heart, Lung and Blood Institute concluded:
Heart failure occurs when an abnormality of cardiac function causes the heart to fail to pump blood at a rate required by the metabolizing tissues or when the heart can do so only with an elevated filling pressure. The heart’s inability to pump a sufficient amount of blood to meet the needs of the body tissues may be due to insufficient or defective cardiac filling and/or impaired contraction and emptying. Compensatory mechanisms increase blood volume and raise cardiac filling pressures, heart rate, and cardiac muscle mass to maintain the heart’s pumping function and cause redistribution of blood flow. Eventually, however, despite these compensatory mechanisms, the ability of the heart to contract and relax declines progressively, and the heart failure worsens.
Because all cardiac diseases have the potential to produce heart failure through similar mechanisms, we frequently view their pathophysiology and therapy from a unified perspective. Agents that promote preload and afterload reduction are used to control the clinical signs associated with elevated filling
Eressures, and neurohormonal modulators are prescribed to lunt the progressive nature of heart disease. This approach allows clinical experience and research to be extrapolated across a wide range of diseases. Although the remainder of this post is written primarily from a unified perspective, caution must be exercised to ensure that the variations within cardiovascular diseases are not forgotten.
Phases Of Heart Failure
Currendy, three distinct phases of heart failure are recognized. Phase 1 constitutes the initial cardiac injury. This phase most frequendy passes silendy, without detectable clinical signs, because compensatory mechanisms (phase 2) are quickly activated. Ultimately, myocardial hypertrophy accounts for the long-term stabilization of cardiac output and the normalization of afterload. Unfortunately, the natural history of cardiac disease often is progressive, and the heart’s ability to hypertrophy is overwhelmed. The previously beneficial short-term compensatory mechanisms now serve only to increase both preload (contributing to the development of congestion) and afterload (increasing myocardial work and oxygen demand). Often a heart murmur, gallop rhythm, cardiac arrhythmia, or cardiomegaly may be identified during this second phase despite the absence of significant or activity-limiting clinical signs. Phase 3 of heart failure is recognized by the emergence of clinical signs (e.g., exercise intolerance, lethargy, coughing, tachypnea) at rest or with minimal activity. Veterinary patients apparendy do not show clinical signs that are recognized by their owners until very late in the disease process. Presumably this may skew our understanding of the natural history of canine and feline cardiovascular disease. This understanding of disease progression is further clouded by the recognition that, depending on the disease process, the first clinical event may be the development of systemic thromboembolism, syncopal episodes, or possibly sudden death.
Natural History Of Cardiovascular Disease
Despite decades of treatment of cardiovascular disease in companion animals, relatively few studies have reported on the survival characteristics of patients afflicted with dilated cardiomyopathy, mitral insufficiency, and hypertrophic cardiomyopathy. The spectrum of clinical signs, therapeutic strategies, breed differences, and disease sequelae hampers the formation of any sweeping conclusions regarding the natural history of these cardiovascular diseases; however, some generalities may be recognized. After dilated cardiomyopathy has been diagnosed, the survival curve drops precipitously for the first 3 months, with median survival times from two retrospective studies reported as 27 days and 65 days. Months 3 through 6 continue to see a large number of dropouts, although interestingly, the curves appear to flatten markedly at approximately 6 months after the initial diagnosis. Whether this represents differences in individual responses to therapy or in the severity of disease at the time of diagnosis is difficult to ascertain.
Analysis of the survival curves for cats with hypertrophic cardiomyopathy presenting with congestive heart failure (CHF) or aortic thromboembolism (ATE) that lived for greater than 24 hours initially showed a steep slope similar to that seen in dogs with dilated cardiomyopathy. Approximately 25% of the congestive heart failure group and 40% of the thromboembolism group died within 3 months of diagnosis. After 3 months, cats presenting for congestive heart failure began to display a less steep, linear survival curve that concluded in a plateau several years after the diagnosis. The survival curve for cats with thromboembolism also displayed some flattening after the first 3 months, although it ukimately remained linear for the rest of the study period. The median survival times were 563 days and 184 days, respectively, for cats with congestive heart failure and those with aortic thromboembolism. Cats with subclinical hypertrophic cardiomyopathy were significantly more likely to die of noncardiac disease (P < 0.001) and displayed a linear mortality curve for the first 4 years, followed by a prolonged plateau for an additional 4 years.
Interestingly, although mitral insufficiency is the most commonly recognized cardiovascular condition in dogs, the natural history and mortality characteristics after the development of congestive heart failure have received little attention. Investigators for the Long-Term Investigation of Veterinary Enalapril (LIVE) study evaluated the time to treatment failure for dogs with congestive heart failure treated with enalapril and standard medical therapy (furosemide with or without digoxin) versus those treated with placebo and standard medical therapy. In the mitral insufficiency subgroup, the number of dogs remaining in the study randomized to placebo mimicked the survival curve of dogs with dilated cardiomyopathy. A relatively high dropout rate was seen over the first 50 days, followed by a prolonged period of stability. The data for dogs randomized to enalapril did not display this steep dropout rate, but rather formed a linear curve from the time of enrollment until completion of the study.
Influences On The Natural History
Unlike in the management of heart disease in humans, veterinary medicine has the profound ability to influence the natural history of cardiovascular disease in companion animals through the use of euthanasia. The ready access to euthanasia in veterinary medicine not only influences patients’ survival times, but also may alter the clinician’s responsibilities in treating the heart failure. A study by Mallery et al. evaluated the factors that contributed to clients’ decision for euthanasia for 38 dogs with congestive heart failure. The most important factors cited were a perceived poor prognosis (37%), recurrent signs of congestive heart failure (26%), and poor quality of life (13%). Common contributing factors included weakness (76%), anorexia (68%), recurrent clinical signs of congestive heart failure (55%), and a poor prognosis (42%). These findings suggest that the goals of the practitioner should include careful client education before and after initiation of medical therapy, along with efforts to improve the patient’s strength, appetite, and quality of life, possibly at the expense of prolonged survival.