Public health

Long COVID breathlessness not linked to heart: study

Breathlessness often experienced by people with long COVID is not explained by a cardiopulmonary cause, a small study by Australian researchers suggests.

Suspicion first fell on cardiopulmonary mechanisms after direct pulmonary pathology was ruled out — with post-COVID lung issues, such as pulmonary fibrosis, reported in some but not all long COVID patients — and a growing body of literature implicating the cardiovascular system in COVID illness.

However, a study led by Professor David Kaye Director of Cardiology and a senior cardiologist in the Heart Failure and Transplant service at the Alfred Hospital Melbourne suggests generalised postcritical illness, and not cardiopulmonary activity, may be driving long COVID dyspnoea.

Published in Circulation: Heart Failure, the study assessed haemodynamic and metabolic profiles of 12 patients presenting to the hospital with post-COVID breathlessness and 12 age-matched healthy volunteers.

It found the patients, who were around 50 years old, slightly heavier than controls and cleared of a pulmonary cause, had “significant functional limitation (7 New York Heart Association III and 5 New York Heart Association II)”.

They also had lower left ventricular ejection fraction at rest (66 ± 5% versus 70 ± 4%, P = 0.03), smaller left ventricular end diastolic index (23 ± 2 versus 25 ± 3 mm/m2, P = 0.03) and diminished work capacity and exercise cardiac index peaks versus controls (58 ± 8 versus 122 ± 13, P < 0.001 and 5.5 ± 0.5 versus 7.2 ± 0.3, P = 0.007, respectively).

Despite this, patients had normal resting haemodynamics, and similar resting and exercise arterial O2 saturation, arterial PCO2 and mixed venous O2 saturation to controls.

“Notably the resting arterial lactate concentration was higher in patients with COVID at rest but given the lower peak workload level rose to a lesser extent during exercise,” Professor Kaye and his team wrote.

Though some patients went without radiological testing for chronic pulmonary thromboembolic disease, “these data would tend to preclude such a diagnosis”.

Therefore, “in this cohort of long COVID patients, we … cannot ascribe a cardiopulmonary cause to the sensation of breathlessness”, they wrote.

What the study lacks in size, it makes up for in strength given by their “detailed invasive [haemodynamic] and echocardiographic assessment at rest and during exercise”, they suggested.

While early reports noted the “frequent occurrence of increased levels of cardiac injury biomarkers particularly in patients with severe COVID illness, potentially due to acute plaque rupture, microvascular damage or myocarditis”, their proposed link to exertional breathlessness remains controversial.

Critical illness is often followed by a “protracted recovery phase, due to acquired respiratory and peripheral muscle weakness, impaired cognition and posttraumatic stress”, and the modestly elevated blood lactate level, which was not associated with exercise, is similar to that seen with chronic fatigue, the authors wrote.

They suggested breathlessness during exercise could be driven by post-viral and postcritical illness changes in autonomic function.

“Taken together, our data are more consistent with long COVID [dyspnoea] being the result of a [generalised] postcritical illness process rather than a primary cardiovascular cause,” they wrote.

Even with the unlikely involvement of central cardiovascular or pulmonary vascular complications, there remains “an important role for comprehensive cardiopulmonary evaluation in patients with unexplained breathlessness, including long COVID”.

“Such an assessment should include cardiopulmonary exercise testing and invasive exercise [haemodynamic] studies,” the authors concluded.

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