A Look Back at "The Management of Heart Failure 5 Years Hence"

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American Heart Hospital Journal 2011;9(2):78-80

It is interesting to look back at our predictions1 to see where we are relative to these forecasts. Five years is not that long ago and so, hopefully, we will be close to the targets we set.


Prevention remains the ultimate approach to managing heart failure (HF). Basically, we are talking about eliminating the risks for left ventricle (LV) dysfunction for the Stage A patient (who has risks for LV dysfunction, but with a normal LV) and eliminating the threatening risks for the Stage B patient (who has asymptomatic LV dysfunction) with the intent of preventing, or at least delaying, the progression of LV dysfunction into symptomatic HF. Unfortunately, our preventive interventions are still blunted by social and economic roadblocks.

More physicians are aware of these risks, but how are we doing? Hypertension awareness in the general public has risen and the need to bring hypertension under control has caught the attention of more practicing physicians. The target blood pressure remains a moving target, but certainly <140 mmHg systolic is a good place to start. Patient compliance, largely related to the cost and convenience of delivering the ideal antihypertensive therapy, is a limiting factor for millions.
The risk of high blood lipids has also attracted public awareness and the attention of practicing physicians. Again, patient adherence to lipid management is often the limiting factor, not only in taking the one or more medications, but also in obtaining the follow-up lipids, liver enzymes, and related studies. Having physicians test for lipids in their adult and adolescent populations is a good start.

Inpatient diabetic control has lightened up somewhat (from strict diabetic management) and outpatient management has benefited from the introduction of new improved agents to provide a wider spectrum of choices and overall better control.

There are data to show that tobacco abuse is slowly dropping, but remains a major threat among many of our young (who will most probably drag smoking into adulthood). Other forms of substance abuse (e.g. alcohol and drugs) remain unchanged in prevalence or, in some circles, slowly growing in popularity.

Obesity is increasing in incidence and prevalence, as are its consequences, hypertension, diabetes mellitus and hyperlipidemia. Certain segments of our society have adopted a more active lifestyle with regular physical activity, but this group is relatively small compared with the obese population. Obesity is becoming a major problem of childhood and adolescence; ‘fast foods,’ snacks, soft drinks, television, and video games are relentless, tough competitors.

The HF population is steadily growing, in part related to the advancing age of our population and to our ability to enhance the survival of the HF patient with β-blockade, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II (AII) antagonists, biventricular pacemakers, and implantable cardioverter-defibrillators (ICDs). Unfortunately, some of the expansion of the HF population is also related to our inability to bring the HF risks for the Stage A and B patients under better control. As predicted, over the past five years we have achieved very little with respect to reducing HF risks. Physicians, the entire spectrum of healthcare providers, and society in general have plenty of work remaining in the common goal of preventing HF.

Diagnostic and Monitoring Modalities

More biomarkers are on the horizon for HF prognostication. It remains to be seen whether any of them are able to improve upon or unseat B-type natriuretic peptide (BNP) as the dominant player in this area.

At this point, the contrast 64-slice computed tomography (CT) scan has impacted the evaluation of peripheral vascular disease more than it has coronary atherosclerosis. We have learned over the past four to five years that the radiation exposure of CT angiography is considerably higher than anticipated, blunting the enthusiasm for the routine use of this diagnostic tool. Magnetic resonance imaging (MRI) has played a greater role in cardiovascular imaging. MRI is now the preferred method for assessing myocardial scarring and viability, ventricular volumes and systolic function, complex congenital cardiac lesions, and peripheral vascular disease. Myocardial evaluation by MRI now also provides information on prognostication, based on the amount of scarring, and information on inflammatory (myocarditis) and infiltrative (amyloidosis) disease; the last feature has reduced the need for myocardial biopsy to establish these diagnoses. At the present time, MRI in the HF patient is restricted to those without an indwelling metallic device (e.g. pacemaker, cardioverter-defibrillator). MRI-compatible devices are under development. Defining coronary anatomy by MRI is still a shortcoming.

As predicted, the use of the flow-directed, Swan-Ganz, pulmonary artery catheter has continued to decline, but there is a tremendous amount of research and activity occurring in the area of indwelling devices for hemodynamic monitoring. Pulmonary artery and left atrial pressures can now be recorded continuously to detect the development of early HF decompensation; early intervention can then be directed at averting symptoms and hospitalization. Success will depend on the development of an infrastructure within hospitals and practices to monitor the hemodynamics from these devices and then institute appropriate therapy. Whether these methods will thrive is linked to their cost-effectiveness: basically, will they prevent enough hospitalizations to offset the cost of the device? Proper patient selection will probably be mandatory.

We have learned more about genetic testing for familial cardiomyopathies. There are now more than 40 genetic defects, alone or in combination, associated with these conditions. This area will continue to attract research to define additional genetic disorders, both in familial and non-familial cardiomyopathy. To address the ‘So what?’ question, the hope is to eventually replace or manipulate the genetic defect once the specific derangement is identified.


As predicted, digoxin utilization has fallen to <30 %, while ACE inhibitors (or AII antagonists) and β-blockade are approaching >90 % of eligible HF patients. The use of aldosterone antagonists is steadily increasing for New York Heart Association functional class (FC) II–IV HF, with hyperkalemia and renal dysfunction restraining some of the enthusiasm for routine use. Administration of aldosterone antagonists requires careful monitoring of serum potassium. Vasopressin antagonists may be helpful for the volume-overloaded hyponatremic patient. To date, endothelin blockers and cytokine inhibitors have not been found to play a major role in HF therapeutics.

We are waiting to see if pharmacogenomics will impact the practice of HF therapeutics.

Other than judicious diuretic administration, and perhaps some β-blockade and an ACE inhibitor to block the renin–angiotensin–aldosterone response to the diuretic, the management of diastolic HF (HF with preserved ejection fraction) remains a challenge, and there is little hovering on the horizon.

Device Intervention

Biventricular pacing for resynchronization of ventricular contraction has impacted HF management, but distinguishing the 65–70 % who will benefit from this intervention from the 30–35 % who will not (or worsen) remains a challenge. We now know that left bundle branch block with a QRS duration of >150 msec has the highest incidence of improvement. However, some of the patients with durations of 120–150 msec will also benefit; but who?

Ultrafiltration provides the most efficient means of removing fluid in a patient with marked volume overload; a reasonable approach for the patient who has a sluggish response to diuretics.

Surgery for Heart Failure

The Surgical treatment for ischemic heart failure (STICH) trial was mired from the start with major difficulties (e.g. recruitment, patient assignment), making the results virtually uninterpretable. Perhaps we learned that surgical ventricular restoration (SVR) of an aneurysmal LV (with or without concomitant mitral valve surgery) was not helpful for the group randomized to SVR, but we all have individual patients who benefited greatly from this procedure. Whether coronary bypass surgery is of benefit to the patient with LV dysfunction-HF (ejection fraction <30 %) secondary to coronary artery disease remains largely unanswered and this approach is now threatened by the continued development of catheter-based coronary interventions.

Left ventricular assist devices (LVADs) are now in the third generation of development. The changes brought about by their continued improvement have greatly reduced the complication rate (e.g. stroke, infection, bleeding) and increased the longevity of the devices. LVAD use is on a steady climb, particularly with the ongoing shortage of donor hearts, the expanded criteria for LVAD candidacy, and for patients awaiting transplantation. Research in this area will continue at a steady pace with the goal set at no embolization, little bleeding, and a self-contained, internal energy source.

Survival following cardiac transplantation is gradually improving to >90 % at one year and >80 % at five years. This has occurred despite our liberalization of recipient criteria to include more comorbidities (e.g. complicated diabetes, peripheral vascular disease). The improved survival is probably related to the increased experience of transplant cardiologists, newer improved immunosuppressant agents (e.g. tacrolimus, anti-thymocyte globulin, sirolimus) and augmented strategies to counter cardiac allograft vasculopathy. We are now expecting most of our transplant patients to survive 10 years following transplant, with a goal of over 20 years.

Stem cell therapy, a form of transplant in most instances, is certainly an intervention of the future. Post-infarction patients will be initially targeted. This area is moving fast, with optimistic hope for the future.

Closing Comments

As noted, our improved therapies and the increasing age of our population are expanding the HF base. While theoretically solvable, the obesity ‘epidemic’ (and associated hypertension and diabetes mellitus) in particular will greatly increase the HF population, by initially adding patients with diastolic dysfunction HF, and will bring this condition into a younger age group.

With respect to our predictions for HF care, made five years ago, we were not too far off—but how could we miss?

  1. Leier CV, Haas GJ, The management of heart failure 5 years hence, Am Heart Hospital J, 2006;4:207–10.