Congestive heart failure

The clinical clues and signs of advanced heart failure

Dr. Mark Drazner
Dr. Mark Drazner

By Mark Drazner, M.D., M.Sc.
Clinical Chief of Cardiology

While there is no universally accepted definition of “advanced heart failure,” one way to identify patients who have this condition is to say they require spe­cialized therapies such as a left ventricular assist device (LVAD) or heart transplantation. Increas­ingly, these patients are treated by cardiologists who have trained an additional 12 months following their general cardiology fellowship. Indeed, the fields of advanced heart failure and transplant cardiology are now recognized as their own American Board of Internal Medicine board-certified subspecialty.

Recognizing the importance of this emerging field, I proposed to the Program Committee of the American Heart Association Scientific Ses­sions that we have a session dedicated to it, and the committee agreed it was a worthy undertak­ing. I was fortunate to have the opportunity to co-moderate that session.

One of the session’s unique features was having a mock selection committee composed of internationally renowned faculty speakers. To my knowledge, this was the first time such an effort was undertaken at the AHA Scientific Sessions.

Two challenging patient scenarios were presented to the selection committee by junior faculty, and the committee members then discussed how they would decide whether such patients would be appropriate candidates for a transplant or LVAD. The goal of the session was for practicing cardiologists, and other advanced heart failure cardiologists, to learn from the thought processes of leaders in the field – in essence, providing a glimpse of some of the behind-the-scenes decision making that occurs in selection committees.

The session’s speakers were outstanding. One of the case presenters noted that our panel members were his heroes from the field of heart transplantation and dubbed them the “Justice League of Heart Transplantation!”

An important concept for practicing cardiolo­gists discussed at the AHA Sessions was how to identify patients with advanced heart failure before they progress to an extreme state of car­diogenic shock. The following are simple clinical clues that can be easily incorporated into everyday practice as triggers for consideration of referral to an advanced heart failure center such as the one we have at UT Southwestern:

  • Two or more hospitalizations for heart failure in 12 months
  • Inability to tolerate ACE-inhibitors, ARBs, or BBL due to hypotension or renal failure
  • Worsening renal function (rising BUN and Cr)
  • Requiring higher doses of diuretics
  • ICD shocks for ventricular tachycardia
  • Loss of body weight from cardiac cachexia
  • Hyponatremia (Na <135)
  • Persistent NYHA class 4 dyspnea (including shortness of breath with dressing or showering)

With earlier identification of advanced heart failure, outcomes undoubtedly will improve because such patients will be in better shape to undergo transplantation or LVAD implantation.

“One of the case presenters noted that our panel members were his heroes from the field of heart transplantation and dubbed them the “Justice League of Heart Transplantation!”

Using low-oxygen therapy to regenerate growth in damaged hearts

Dr. Hesham Sadek
Dr. Hesham Sadek

By Hesham Sadek, M.D., Ph.D.
Associate Professor of Internal Medicine

Our team recently completed a regenera­tion biology study that further investi­gated neonatal heart regeneration in mice. With this information and future research, we hope to one day reverse the damage from myocardial infarction and other heart conditions in human hearts through the use of low-oxygen therapy.

We began this research in 2011 with a study published in Science that demonstrated the ability of myocytes in neonatal mouse hearts to regenerate after damage. However, this period of regeneration is limited to a small window of just a few days after birth due to the development of an oxygen metabolism that delivers ample oxygen to the cells. This change in metabolism shuts down the heart’s regenerative abilities. We published this finding in Cell in 2014. 

However, subsequent findings published in 2015 in Nature indicated that a few heart cells with exceedingly low oxygen pockets retain the ability to divide. Our most recent research, published in November 2016 in Nature, indicates that the hearts of adult mice can regenerate through controlled oxygen intake in a hypoxic chamber. For this study, we induced myocardial infarction in mice, waited for injury to be established, and measured the regenerative capabilities of their hearts as we gradually lowered the oxygen in their air supply to 7 percent – approximately the oxygen level at the top of Mt. Everest. 

After two weeks in the hypoxic environ­ment, the cardiomyocytes began to regenerate. This is encouraging because in environments with normal oxygen levels, cardiomyocyte regeneration does not occur in adult mammals.

Our next step is to consider how to use hypoxic conditions to repair myocardial infarction damage to the human heart. The promising results in our mouse test subjects give us solid footing to focus on developing effective therapies for human infants and adults.

“After two weeks in the hypoxic environ­ment, the cardio­myocytes began to regenerate. This is encouraging because in environments with normal oxygen levels, cardiomyocyte regen­eration does not occur in adult mammels.” 

Exercise intolerance in heart patients: chronotropic incompetence or chronotropic reluctance?

Dr. Satyam Sarma
Dr. Satyam Sarma

By Satyam Sarma, M.D.
Assistant Professor of Internal Medicine

Nearly half of heart failure patients receive a diagnosis of heart failure with pre­served ejection fraction, or HFpEF.Currently, no treatment options exist for these patients, unlike for those diagnosed with heart failure with reduced ejection fraction.

Better understanding of the pathologic abnormalities causing HFpEF may lead to more effective therapies. One of HFpEF’s key hallmarks is severe exercise intolerance. Chronotropic incompetence, or the inability to increase heart rate, is widely thought to be the reason, as this inability limits aerobic capacity by hindering further increases in cardiac output. 

A number of studies have linked chrono­tropic incompetence with low VO2 max (the maximum volume of oxygen a person can use) in HFpEF patients and have even advocated implantation of rate-responsive pacemakers to improve exercise tolerance

Our study challenged the causes of chrono­tropic incompetence in HFpEF. We hypothesized the determinants of heart rate response during exercise – cardiac beta-receptor sensitivity and central command – would be normal in patients with HFpEF.

Using an autonomic blockade to prevent reflexive tachycardia, our study found cardiac beta-receptor stimulation to isoproterenol was normal in HFpEF patients compared to similar age- and gender-matched controls. Our findings suggest the presence of chronotropic incompe­tence may not reflect sinus node dysfunction but rather premature cessation of exercise, possibly due to symptoms of dyspnea.

“Our study challenged the causes of chrono­tropic incompetence in HFpEF. We hypothe­sized the determinants of heart rate response during exercise – cardiac beta-receptor sensitivity and central command – would be normal in patients with HFpEF.”

Exercise to prevent heart failure with preserved ejection fraction

Dr. Ambarish Pandey
Dr. Ambarish Pandey

By Ambarish Pandey, M.D.
Clinical Fellow, Division of Cardiology

Heart failure (HF) affects approximately 5.8 million people in the U.S. and accounts for an estimated annual health care cost of $34.8 billion. While the incidence of athero­sclerotic cardiovascular disease has decreased steadily over the past 40 years, the burden of HF has remained largely unchanged. 

Moreover, all of the advances in HF therapy over the last quarter century have been limited to patients who have HF with reduced ejection fraction (systolic HF). In contrast, multiple recent trials have failed to improve clinical outcomes for patients who have HF with preserved ejection fraction (diastolic HF). This highlights the critical need for cost-effective, preventive interventions to address HF with preserved ejection fraction.

An important step in HF prevention is identi­fying modifiable risk factors that can be targeted with effective preventive strategies. Lifestyle risk factors such as physical inactivity and obesity have been demonstrated to play an important role in HF development. 

Our study evaluated the dose-response relationship between physical activity levels, body mass index, and HF risk with preserved and reduced ejection fraction using individual-level pooled data from three well-characterized pro­spective cohort studies. We observed a significant dose-dependent inverse association between higher levels of leisure time physical activity and HF risk, with a more consistent and graded as­sociation for HF with preserved ejection fraction versus HF with reduced ejection fraction.

Additionally, we observed that higher levels of body mass index above normal range are asso­ciated with increased HF risk. This relationship is stronger and more graded for HF with preserved ejection fraction than it is for HF with reduced ejection fraction. 

These findings suggest the possible preventive role of lifestyle patterns for HF with preserved ejection fraction. In addition, these findings could have implications for future guidelines aimed at the prevention of HF with preserved ejection fraction in the general population. Adequately designed randomized prevention trials are needed to further evaluate this hypothesis and determine its implications for clinical and public health practice.

“Multiple recent trials have failed to improve clinical outcomes for patients who have HF with preserved ejection fraction. This highlights the critical need for cost-effective, preventive interventions.”

 

Physician Referral Information

UT Southwestern welcomes referrals from providers seeking optimal care for heart patients. Physicians and offices can refer a patient with one easy call to the heart intake coordinator, a registered nurse who is available 24 hours a day, seven days a week. Same-day access is available for patients experiencing chest pain and chest discomfort. To refer a patient to any UT Southwestern clinic or for general inquiries, call Patient and Physician Referral Services at 214-645-8300.

Clinical Heart Center Patient Referrals

Phone: 855-240-0816
Fax: 214-645-7269

Questions or Comments

If you have any questions or would like more information about the Clinical Heart Center or the recent AHA Scientific Sessions, contact Dr. Mark Drazner, Clinical Chief of Cardiology, at mark.drazner@utsouthwestern.edu.

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