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Heart Failure with Preserved Ejection Fraction

The fifth episode features Geoffrey Mills, MD, PhD, covering heart failure with preserved ejection fraction, including the following topics

• Heart failure with preserved ejection fraction versus heart failure with reduced ejection fraction
• The difference between heart failure with preserved ejection fraction and diastolic dysfunction
• Treatment of heart failure with preserved ejection fraction

Featured Physician

Geoffrey Mills, MD, PhD
Assistant Residency Program Director, Assistant Professor
Department of Family and Community Medicine and Department of Physiology
Jefferson Medical College, Philadelphia, PA

Dr. Mills is a graduate of Temple University School of Medicine and did his Family Medicine training at Thomas Jefferson University Hospital in Philadelphia. He has a research background in cardiovascular physiology and has a dual appointment in the Departments of Family and Community Medicine and Department of Physiology at Jefferson Medical College. His teaching and clinical interests relate to cardiovascular disease and preventative medicine and he studies risk communication in primary care.

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Transcript:

Joining us today is Geoffrey Mills MD, PhD. Doctor, why did you choose heart failure with preserved ejection fraction as the topic for this month’s podcast?

Physicians are familiar with managing congestive heart failure – common symptoms and treatment approaches – but less familiar with the differences in treatment and management of patients exhibiting symptoms of heart failure, but with preserved left ventricular function.  Unfortunately, at this point, there are few large, high-quality trials available to guide treatment decisions in this patient population, so physicians often apply principles most appropriate for patients with reduced ejection fraction.  With our aging population, we will be seeing more HF with preserved ejection fraction so physicians should be comfortable identifying this condition.

What is the difference between heart failure with preserved ejection fraction and diastolic heart failure?

HF with preserved ejection fraction is the preferred terminology for diastolic heart failure.  There is an important distinction between HFPEF and diastolic dysfunction, which is often a finding on routine echocardiograms.  Diastolic dysfunction refers to an abnormality of diastolic compliance, filling or relaxation of the ventricle.  This can occur in the absence of symptoms classically associated with heart failure – shortness of breath, fatigue and volume overload.  If these signs and symptoms are present in a patient with a normal ejection fraction, they are said to have HFPEF.  Usually, you will find some evidence of diastolic dysfunction in these patients as well.

Who is most at risk to develop this condition?

When compared with HFREF, patients with preserved ejection fraction are older, more likely female and usually have a history of hypertension.  They are also more likely to have atrial fibrillation but less likely to have a history ischemic disease, although coronary artery disease is a common co-morbidity.  They have similar symptoms as those with reduced ejection fraction like reduced exercise capacity and reduced quality of life.  In patients presenting with these symptoms, consider HFPEF in your differential diagnoses, especially for older women with a history of long-standing hypertension.

Acute exacerbations of HFPEF cause the classic HF symptoms of fluid overload and chest pain in patients.  These flare-ups are most commonly triggered by hypertensive crises but can also be due to tachycardia, especially atrial fibrillation, renal impairment or other acute illnesses.

What is the course of HFPEF?

HFPEF is a chronic disease for most patients with a slow progression and occasional exacerbations.  Unfortunately, the presence of diastolic dysfunction by itself is associated with increased risk of cardiovascular events.  There is some controversy about whether there is a difference in the mortality rates between patients with HFPEF and HFREF but it is generally accepted that patients with HFPEF who are male, higher NHYA classification, ischemic disease or impaired renal function fare worse than other patients.

HFPEF is a chronic disease and physicians should aim to control hypertension, ventricular rate, fluid balance and, in some patients, consider revascularization.  Patients should be instructed in self-care behaviors like daily weights and medication adherence as well as dietary sodium restriction.

How should clinicians approach the treatment of HFPEF?

As I mentioned, the main treatment goals are treating hypertension, maintaining a normal heart rate and keeping the patient euvolemic.  The challenge in HFPEF is that there are few clinical trials demonstrating meaningful benefits in morbidity and mortality to guide the choice of pharmacologic agents.  For instance, ACE inhibitors and angiotensin receptor blockers can improve diastolic function and may improve functional class and exercise capacity but there is limited data showing improvements in morbidity and mortality.  Both are reasonable choices for blood pressure control, especially for patients with LV hypertrophy but they should not be used in combination.

Beta blockers can help in two ways: blood pressure control and heart rate control. Again, evidence for improved morbidity and mortality is lacking, but some trials have suggested benefits for this group of patients.  If we project treatment recommendations for patients with reduced ejection fraction, carvedilol, long-acting metoprolol and bisoprolol seem most promising for use in these patients until new data are available.

Calcium channel blockers will also help with hypertension and heart rate in these patients and may, in theory, improve diastolic function.  Verapamil has been shown in small studies to improve exercise capacity and HF symptoms in HFPEF.

New trials are looking at the role of aldosterone antagonist therapy in HFPEF with early studies suggesting that they may improve myocardial function.  Until more data are available, these drugs are not generally recommended for patients with preserved EF.

Diuretics such as furosemide are used in acute exacerbations to improve fluid overload but may be necessary in some patients to maintain fluid balance chronically.

I hope that we will have some more data to help guide these treatment decisions in this patient population, but until that time, most of our treatment options are drawn from studies in patients with reduced ejection fraction.

How is this different from heart failure with reduced ejection fraction?  Are there unique treatment considerations?

One unique difference is that patients with HFPEF seem to tolerate the initiation of beta blockers and calcium channel blockers during acute exacerbations.  Patients with systolic HF generally are not started on new beta blockers during acute exacerbations for fear of depressed contractility.  So, when heart rate control is needed, these agents can be used, even during acute exacerbations.  Another difference is that inotropic agents like digoxin and dobutamine are not indicated for use in acute or chronic HFPEF.  Finally, patients who are very sensitive to tachycardia from atrial fibrillation should be considered for rhythm control strategies to maintain sinus rhythm.  Guidelines also suggest that coronary revascularization should be considered in patients with CAD and diastolic dysfunction.

Are there particular lifestyle recommendations that patients should follow?

Weight loss, smoking cessation and dietary changes should be discussed with patients to reduce ischemic risk and improve blood pressure control.  Dietary sodium restriction to less than 2 grams per day will reduce mean arterial blood pressure and may prevent hypokalemia in patients on diuretics – I would recommend the sodium-restricted DASH diet, which has been shown to reduce blood pressure and improve exercise tolerance in patients with HFPEF.

Most patients should monitor daily weights and have some plan in place for what to do if they begin to gain weight or have symptoms of heart failure.  This type of action planning is a good way to engage patients in their medical care and can reduce the risk of hospitalization.  In addition, exercise training can improve functional capacity in patients with HFPEF – some areas will have access to cardiac rehabilitation services but most patients can safely participate in moderate intensity aerobic exercise 3-5 times per week.

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Abdominal Aortic Aneurysm

The fourth episode features Bon Ku, MD covering abdominal aortic aneurysm or AAA, including the following:

• Risk Factors for developing AAA
• Presentation of AAA and reliable screening
• Ultrasound and accurate diagnosis

FEATURED PHYSICIAN

Bon Ku, MD
Assistant Professor in the Department of Emergency Medicine
Thomas Jefferson University Hospital

Dr. Ku completed a fellowship in emergency ultrasound at the Hospital of the University of Pennsylvania and received a Master in Public Policy at the Woodrow Wilson School of Public and International Affairs at Princeton University. He graduated from the Penn State College of Medicine and completed an emergency medicine residency at Long Island Jewish Hospital. His research areas of focus are point-of-care ultrasound, utilization patterns of emergency departments and homeless populations.

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Transcript:

Thank you for being here today, Dr. Ku. Why did you choose abdominal aortic aneurysm (AAA) as the topic for this month’s podcast?

A ruptured AAA is a vascular catastrophe, responsible for 9,000 deaths yearly in the US. The prevalence of AAA ranges from 4-8% in males and 1% in females. It is a silent killer because patients often are asymptomatic until the aneurysm ruptures. Once ruptured, the mortality is greater than 80%. Because the mortality rate is so high, a rapid diagnosis of AAA may be lifesaving.

How reliable is the physical exam in diagnosing AAA?

Terrible. We physicians do a poor job at detecting its presence by physical examination. The odds of ruling out the presence of a AAA by palpation is like flipping a coin. Published reports have sensitivities ranging from 29-76%1 and the specificities are only slightly higher. There are a large number of false positives and false negatives, resulting in a poor predictive value2. Because abdominal palpitation has a low sensitivity for detecting aneurysms, especially ones <5 cm, I would argue that the physical exam should not play a role in ruling out AAA.

What imaging modality should be used as the first line of screening for detecting AAA?

Unequivocally ultrasound. Ultrasound for the detection of AAA has been shown to have a 95% sensitivity and a specificity approaching 100%. It is safe, non-invasive, cost-effective and can be performed quickly in emergent settings right at the patient’s bedside. A complete aorta scan can be completed in just over 2 minutes. In my current practice, I use ultrasound as a rapid point-of-care test for ruling out AAA in a similar fashion to how I use an EKG to rule out an acute myocardial infarction.

Who is at most risk for developing AAA?

The greatest risk factors are age greater than 65 years, male sex, and smoking. Other risk factors for AAA include a family history of AAA and atherosclerotic risk factors. In 2005, the U.S. Preventive Services Task Force made a Class B recommendation that men between the ages of 65-75 who have ever smoked should receive a one-time screening ultrasound. The UK has similar screening guidelines.

Does routine screening for AAA occur in Emergency Departments?

No. But one study suggested that EDs may provide an opportunity to screen asymptomatic, high-risk patients for AAA 3. The investigators found a 6.7% prevalence of AAA in a sample size of 179 patients who were >60 years, male and had at least 1 risk factor for AAA.

How does a patient with a ruptured AAA present?

We have been taught that patients present with the classic triad of abdominal pain, pulsatile abdominal mass, and hypotension. But patients rarely show all these telltale signs. Patients often have non-specific symptoms ranging from flank to back pain or syncope. A 30% misdiagnosis rate for ruptured AAA has been previously reported 4. The most common wrong diagnoses for ruptured AAA are renal colic, diverticulitis and gastrointestinal hemorrhage.

Where do most aneurysms rupture?

80% of abdominal aneurysms rupture into the retroperitoneal cavity while 20% rupture anteriorly into the peritoneal cavity. In rare cases, AAA can rupture into the IVC or the left renal vein causing spontaneous fistula formation 5. In rare instances, patients can have a delayed presentation of a ruptured aneurysm. This happens when a hematoma forms from a slow rupture. Contained ruptures, however, are at a high risk for spontaneous re-bleeding.

Who should receive an emergent point-of-care ultrasound?

There are 2 groups of patients who should receive an immediate ultrasound in the ED or in-patient hospital setting. The first group includes anyone with a major risk factor for AAA (male, age >65 years, or smoking use) with a suspicion for AAA. The other group of patients are those who have hypotension or shock of unknown etiology. “Rapid Ultrasound in Shock” aka “RUSH” is a protocol that involves the use of point-of-care ultrasound in evaluation of patients in shock. The RUSH protocol entails the following steps: evaluation of aorta size, a focused cardiac evaluation, IVC assessment, FAST, and lung exam for pneumothorax and pulmonary edema 6.

 How do you perform a point-of-care ultrasound evaluation for AAA?

A focused ultrasound exam for the evaluation of AAA involves real-time scanning of the entire aorta from the diaphragm to the iliac bifurcation in the transverse plane. The American College of Emergency Physicians recommends measuring the maximal aortic and iliac size — from outer wall to outer wall — in both the transverse and longitudinal planes. As stated before, ultrasound is extremely accurate in detection of AAA but it cannot be used to diagnose a ruptured aneurysm. Ultrasound is unable to reliably identify the presence of retroperitoneal fluid. Also it is important to keep in mind that the major technical limitations in examining the aorta are obesity, bowel gas and abdominal tenderness.

Referenced Sources

Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal aortic aneurysm? JAMA. 1999 Jan 6;281(1):77-82.

Van der Vliet JA, Boll AP. Abdominal aortic aneurysm. Lancet. 1997 Mar
22;349(9055):863-6.

Moore CL, Holliday RS, Hwang JQ, Osborne MR. Screening for abdominal aortic aneurysm in asymptomatic at-risk patients using emergency ultrasound. Am J Emerg Med. 2008 Oct;26(8):883-7.

Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg.1992 Jul;16(1):17-22.

Assar AN, Zarins CK. Ruptured abdominal aortic aneurysm: a surgical emergency with many clinical presentations. Postgrad Med J. 2009 May;85(1003):268-732

Seif D, Perera P, Mailhot T, Riley D, Mandavia D. Bedside Ultrasound in
Resuscitation and the Rapid Ultrasound in Shock Protocol. Critical Care Research and Practice. 2012.