director, Heart Failure

 by Goldberg and colleagues, it seems reasonable to request a change in the title to "Survival after 

 &#8198;heart failure." Such a change would emphasize that heart failure is a chronic disease that must be vigilantly managed by both patient and physician to limit the extensive morbidity and mortality of the seemingly compensated individual.

Title aside, the article makes clear the challenging fight for survival faced by heart failure patients once hospitalized with an acute decompensation.

 Even after removing the presumably more critically ill 4% that succumbs to in-hospital death, survival after a hospital admission for heart failure is a dismal 63% at 1 year and 21% at 5 years. This bleak prognosis vies with the most malignant forms of cancer (

Although not earth-shattering to the grizzled heart failure specialist, these mortality statistics may be striking to other physicians in the wake of nearly 3 decades of cardiologists trumpeting the dramatic advancements in both the diagnosis and treatment of heart failure patients (

). So where are the advantages we have painstakingly achieved? What happened to the mortality reductions of 16% with the use of angiotensin-converting enzyme (ACE) inhibitors,

 30% reduction with aldosterone antagonists,

 36% reduction with biventricular pacemakers,

 and 23% reduction with implantable cardiac defibrillators?

 Comparison of 1- and 5-year survival after 

            hospitalization for heart failure.

 Cumulative mortality rates for subjects enrolled in chronic heart 

 Percentages of study patients in each heart failure 

            classification. NYHA indicates New York Heart Association functional class. 

Perhaps circumstances preceding hospitalizations can offer clues. The Acute Decompensated Heart Failure National Registry (ADHERE) has quite disturbingly shown that many heart failure patients fail to receive optimal medications prior to their decompensation and hospitalization. More than 40% are not receiving ACE inhibitors or angiotensin II receptor blockers, and more than 30% are not receiving beta blockers.

 In addition, multiple avenues exist for medication failure, even if prescribed: noncompliance, the lack of effective long-term outpatient monitoring, and the readiness with which heart failure patients are dismissed as intolerant of potentially life-saving therapies. Moreover, there exists little economic incentive for physicians to rigorously monitor their heart failure patients for the early stages of decompensation, hyperkalemia, and renal failure.

What about the long-term mortality ramifications of actions taken during the acute hospitalization? Although more than 90% of heart failure patients are hospitalized with volume overload, less than 50% lose more than 5 pounds during the acute hospitalization.

 This may reflect the difficulty in clinically assessing persistent volume overload

 or the fear of inducing renal dysfunction in a patient population where renal function predicts not only in-hospital but also long-term mortality.

 It is therefore surprising that no technologically pragmatic application exists to guide the aggressiveness of diuresis or to gauge when euvolemia has been established.

 Cumulative mortality rates for subjects enrolled in acute or severe 

            decompensation heart failure studies. NYHA indicates New York Heart Association 

It is also sobering to know that, despite a plethora of studies guiding our outpatient treatment, currently no category IA evidence (evidence obtained from systematic review of meta-analysis of randomized, controlled trials) exists to guide the therapy of acutely decompensated heart failure patients. There are no prospective, double-blind, placebo-controlled studies that have shown the benefit of any medication used in the treatment of acutely decompensated heart failure patients to improve 1-, 3-, or 5-year mortality.

 The lack of answers to fundamental questions, including the initial dose and type of diuretics, the optimal method of volume removal, and the role of vasodilators or inotropes, undermines our ability to institute effective therapy. The complexity of trying to solve acute hemodynamic and volume issues while also paying attention to the long-term effects of the acute neurohumoral activation

 is daunting and may be responsible for the lack of mortality benefits with newer diuretics, despite their enhanced early diuresis.

An additional variable is the hospital presentation of the heart failure patient. Although heart failure maybe the primary cause of the hospitalization, it may also appear as acomorbid diagnosis associated with disease states that may be relatively more or less lethal. Cancer, gastrointestinal disease, chronic obstructive pulmonary disease, and sepsis are common cotravelers. In addition, heart failure decompensation in the setting of ischemia, atrial fibrillation, renal dysfunction, and shock result in a call for differential therapies.

The high mortality rates after a hospitalization associated with heart failure require that all aspects of the heart failure admission—from presentation, to medical optimization, discharge, and follow-up&mdash;undergo prospective evaluation to better understand the factors that contribute to the significant mortality associated with progressive pump failure and sudden death.

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When considering the article by Goldberg and colleagues, it seems reasonable to request a change in the title to "Survival after the diagnosis of &#8198;heart failure."

The cost of failure

Despite advances in echocardiography, magnetic resonance imaging, and the ability to perform an endomyocardial biopsy, the underlying etiology of nonischemic left ventricular (LV) dysfunction often eludes clinical detection.

 Takotsubo syndrome (also called apical ballooning) is a unique form of cardiomyopathy that tantalizes us with a rare glimpse into both the etiology and potential reversibility of myocardial dysfunction based on its association with adrenergic activation and its characteristic echocardiographic or ventriculographic appearance.

 Although undoubtedly misdiagnosed as focal myocarditis or vasospasm prior to its description in a 1990 textbook by Sato,

 our appreciation for the existence of Takotsubo syndrome has escalated in tandem with our desire to understand its underlying cause (

). Takotsubo syndrome typically presents in a postmenopausal, emotionally or physically distressed woman reporting acute chest pain or dyspnea, and manifesting mild enzymatic evidence of myocardial damage. Clinically, it may mimic an acute myocardial infarction or ventricular tachycardia. Although angiography reveals the absence of significant epicardial coronary artery disease, echocardiography or ventriculography reveal an end-systolic ventricular “ballooning” that may be heterogeneous.

 The syndrome is strikingly reminiscent of conditions seen in experimental animals that occur after acute increases in afterload or with catecholamine excess. Indeed, both an intraventricular pressure gradient and catecholamine excess have been described in Takotsubo patients.

 Since additional mechanisms remain under consideration, including transient myocardial ischemia due to coronary vasospasm or difficult-to-detect thrombus in the territory of a “wrap around” left anterior descending artery (with its perfusion territory beyond the usual detection abilities of coronary angiography),

 microcirculatory abnormalities, and even genetic predilections, it would be reasonable to assume that multiple forms of the disease may exist. 

 for precise diagnostic criteria for Takotsubo cardiomyopathy for both clinical and basic science investigation.

 The indolent presentation in this case report (progressive fatigue, dyspnea on exertion, and bilateral lower extremity swelling) is less common than the more fulminant presentation marked by acute dyspnea, chest pain, and often, cardiac arrest. The history also reveals the presence of celiac sprue, which raises the possibility that the cardiomyopathy may have been triggered by an electrolyte deficiency

 Electrocardiographic abnormalities, mimicking an acute inferior wall myocardial infarction, were present and the combination of echocardiography and ventriculography revealed apical akinesis with midventricular hyperkinesis. Classically, no angiographic evidence of an obstructive coronary lesion was present. However, we are not told if states of adrenergic excess, including pheochromocytoma or central nervous system disorders, were ruled out. Moreover, we are not told of the follow-up for this patient and potential reversibility of the LV dysfunction. Classic Takotsubo cardiomyopathy is associated with recovery of LV function, usually within 2-4 weeks of presentation. 

 Many questions concerning Takotsubo cardiomyopathy remain for both clinical and basic science researchers. These include an understanding of the heterogeneity of presentation, the optimal nature and duration of treatment, and whether the unique properties of Takotsubo cardiomyopathy will offer a window to more fully understand other forms of cardiomyopathy. 

director, Heart Failure

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