Different heart failure phenotypes of valvular heart disease: the role of mitochondrial dysfunction

Dear Doctor: What Is High-output Heart Failure, And How Is It Treated?

DEAR DR. ROACH: My husband is 73 and was diagnosed with heart failure and a severely dilated left ventricle. At the time, he was pumping 10 liters per minute. He had a proBNP natriuretic peptide level over 10,000 and an ejection fraction of 39%. Later, he was found to have an abdominal arteriovenous malformation (AVM). He underwent three radiological procedures to reduce the size of the AVM.

One year post-procedure, his cardiac output was 5.7 liters per minute; his proBNP level was 1,300; and his ejection fraction was 54%. Clearly, the AVM was the source of the high-output congestive heart failure, and the three embolization procedures were effective. All his symptoms disappeared after the procedures, and he feels stronger and more vital than he has in years. He hikes several miles daily, bikes occasionally, and is able to climb a sand dune without getting winded.

My question is: Does he still have a high-output diagnosis if his heart is pumping at 5.7 liters per minute? If so, what is the proper treatment for someone with this condition? He is currently being treated with minimal doses of lisinopril and Coreg. He would like to know if the dilation to his left ventricle is permanent or will diminish over time. -- K.B.

ANSWER: Heart failure is simply when the heart is unable to pump all the blood it needs to meet the body's demands. Heart failure is broken down into big two categories based on the ejection fraction (EF) of the heart, which is the percentage of blood that the left ventricle squeezes out during each beat.

The EF is normally 50% to 75%, so heart failure with an EF of less than 50% is heart failure with reduced ejection fraction (HFrEF). Meanwhile, if a person has heart failure symptoms and an ejection fraction of 50% or greater, it's heart failure with preserved ejection fraction (HFpEF).

Most cases of heart failure are due to heart disease from longstanding high blood pressure levels, repeated heart attacks, or a condition called idiopathic dilated cardiomyopathy. Your husband has a less-common cause called high-output heart failure. In his case, he has an AVM. This is a direct connection of the arteries and veins that usually occurs in the colon but can be found in other places within the gastrointestinal tract.

You can think of it as a short-circuit of the blood supply; all the oxygenated blood going through the AVM does no good at all, and the heart has to work extra hard to provide the blood that the rest of the body needs. Closing the AVM by blocking it up stops the short-circuit so the heart doesn't have to work as hard.

The best news for your husband is that his symptoms are better. But it's also great that his ejection fraction is now in the normal range and that his BNP is better. Of course, 1,300 is still very abnormal, but it's much better than 10,000.

It takes time for the heart to recover from high-output heart failure. I don't know if there still is some blood going through his AVM, but based on his symptoms, I am optimistic that most, if not all, of the underlying cause is gone. Lisinopril and carvidolol (Coreg) are very standard treatments for heart failure and help to protect the heart.

* * *

Dr. Roach regrets that he is unable to answer individual letters, but will incorporate them in the column whenever possible. Readers may email questions to ToYourGoodHealth@med.Cornell.Edu or send mail to 628 Virginia Dr., Orlando, FL 32803.

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Heart Failure With Preserved Ejection Fraction Underdiagnosed

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Rheumatoid Arthritis Boosts Risk For Heart Failure, But Not Every Kind

Rates of heart failure with preserved ejection fraction (HFpEF) were doubled in patients with rheumatoid arthritis (RA) relative to other people of the same age and sex, researchers found.

On the other hand, risk for heart failure with reduced ejection fraction (HFrEF) wasn't significantly higher in the RA patients, according to Katherine Liao, MD, MPH, of Brigham and Women's Hospital in Boston, and colleagues.

With 1,445 RA patients and 4,335 matched controls and adjusting for standard cardiovascular risk factors, the hazard ratio for HFpEF was 1.99 in RA patients (95% CI 1.43-2.77), while the corresponding estimate for HFrEF was 1.45 (95% CI 0.81-2.60), the researchers reported in Arthritis Care & Research.

While an increased risk for HF overall had been well documented previously, few studies had examined whether it differed according to HF subtype. In the earlier work, the group explained, "HF was generally studied as a single entity and the differential risk of HF subtypes were limited due to the need for large RA cohorts with detailed clinical documentation of phenotypic data (i.E., echocardiograms, cardiology notes)."

But recent evidence around HFpEF -- which is marked by increased ventricular stiffness, reducing fill volume, rather than weakening outflow, as in HFrEF -- has implicated inflammation as a causative factor. Since RA is a systemic inflammatory disease, it made sense to suspect that it might preferentially boost HFpEF.

Liao and colleagues drew on data from the Mass General Brigham (MGB) Biobank, which has enrolled some 115,000 patients from the Harvard-affiliated Massachusetts General Hospital and Brigham and Women's Hospital. RA cases were identified from diagnostic codes and key words and terms elsewhere in patients' records, and the first recorded date for an RA diagnostic code became the index date for each case, if followed by another such code within 6 months. Each case was then matched with three non-RA patients by age, sex, and year of entry into the records system; the index date for controls was a clinical encounter close to that of the corresponding case. Participants already with HF at the index date were excluded.

Mean patient age at the index date was about 51 and 79% were women. Roughly 85% were white. Only 11% of the RA cases were using tumor necrosis factor inhibitors and 3% were on other advanced therapies, while from one-third to one-half were on steroids, methotrexate, or other conventional anti-rheumatic drugs.

HFpEF was defined as HF with ejection fraction ≥50%, while ejection fraction ≤40% was HFrEF; values in between were considered HF with moderately reduced ejection fraction. This latter group wasn't included in the analysis of HF subtypes, but it was counted in results for overall HF.

Among the 1,445 RA cases, 92 developed some type of HF during a median of 10.3 years of follow-up, as compared with 157 of the 4,335 controls (HR 1.79, 95% CI 1.38-2.32, after adjustment for cardiovascular risk factors). HFpEF was the dominant subtype in both RA patients and controls, accounting for 65% of HF cases in the former group and 59% in the latter.

Besides RA, other variables also appearing to raise rates of HFpEF were those commonly identified as risk factors: age, overweight/obesity, diabetes, hypertension, atrial fibrillation, and existing coronary artery disease. On the other hand, although chronic kidney disease also appears on lists of HFpEF risk factors, it wasn't one in the current data, with hazard ratios around 1.20 in RA patients and controls alike that did not approach statistical significance.

"RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF," Liao and colleagues concluded. "Since inflammation is modifiable with anti-inflammatory medications, further studies are needed to determine whether anti-inflammatory therapies have the potential to reduce risk of HFpEF in RA and other individuals with chronic inflammation."

Limitations to the study included its reliance on the MGB Biobank, whose participants may not be reflective of the general population (either for RA patients or overall). Also, the researchers noted, the study didn't account for post-baseline variables like drug treatments started during follow-up, nor did it consider RA disease activity.

If patients went outside the MGB system for cardiac care, HF diagnoses and subtyping would not be included in the Biobank records. Liao and colleagues acknowledged, too, that diagnostic codes aren't always reliable.

John Gever was Managing Editor from 2014 to 2021; he is now a regular contributor.

Disclosures

The study was funded from National Institutes of Health grants.

Liao reported a relationship with UpToDate but no other relevant financial interests.

Co-authors reported relationships with industry.

Primary Source

Arthritis Care & Research

Source Reference: Kawano Y, et al "Risk of incident heart failure and heart failure subtypes in patients with rheumatoid arthritis" Arthritis Care Res 2024; DOI: 10.1002/acr.25481.

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