A strong heart is vital to your health. Lack of cardiac strength is exactly what causes people with heart failure to deteriorate so rapidly. For decades, digoxin has been the most commonly used heart-strengthening drug but a recently published study has shed light a whole new heart-boosting compound that is particularly interesting because it reduces mortality, strengthens the heart, and does not appear to have side effects.
The heart is by far our most important organ, as it supplies the entire body with blood and oxygen. The heart muscle requires enormous amounts of energy to contract rhythmically, day and night. People with heart failure deteriorate rapidly because their heart cannot perform. For this reason they are often treated with so-called inotropic drugs - drugs that affect muscle contraction, namely contraction of the heart muscle. Positive inotropes increase the contractility of the heart muscle, whereas negative inotropes do the opposite, causing the heart to relax. According to the current US and European heart failure guidelines, digoxin is the only positive inotrope that is considered, simply because it does not increase mortality and actually reduces hospital admission associated with a worsening of heart failure symptoms.
A new player
Interestingly, a whole new player has appeared on the field. It is a natural compound called coenzyme Q10 and has been shown to increase cardiac strength and lower heart-related mortality. A recently published study, Q-Symbio, made headlines worldwide by demonstrating how this naturally occurring, vitamin-like compound saved lives and restored strength in failing hearts. There were 43% fewer heart-related deaths among those participants who took a 3 x 100 mg daily dose of coenzyme Q10, compared with those who were given inert dummy capsules (placebo). In addition, there was a massive reduction in hospitalization rates in the coenzyme Q10 group.
Enough to change recommendations?
The big question is whether this study delivers enough clinical evidence to change the existing guidelines for heart failure treatment? Lead investigator of the Q-Symbio trial, Chief Physician Svend Aage Mortensen, MD, a cardiologist with the Heart Center, Department of Cardiology, Copenhagen University Hospital, Denmark, has looked into this and underlines one of the most important virtues of coenzyme Q10, besides it documented efficacy - the excellent safety of the substance. Where digoxin has a limited margin of safety, coenzyme Q10 is "safe and may be described as an indirect positive inotrope by virtue of its restoration of energy production in the mitochondria, leading to improved myocardial performance and outcome in heart failure", as Dr. Mortensen writes in a recent follow-up article1
Several valid arguments
There seems to be several valid arguments for introducing coenzyme Q10 as an adjuvant in heart failure, namely because of the safety and efficacy of the compound, but are these obvious advantages overshadowed by the limited number of participants in the Q-Symbio study? Does a total of 420 patients provide enough support?
To answer that question, Dr. Mortensen points to the year 1987 where the ACE-inhibitor enalapril was recommended in new heart failure guidelines. The scientific underpinning for using this drug in heart failure was a study of 253 patients. If this could provide guideline-changing evidence nearly 30 years ago, why should a well-designed study of 420 patients not be able to do the same today?
Source: The Mitochondria in Heart Failure: A Target for Coenzyme Q10 Therapy? Clinical Pharmacology & Therapeutics | VOLUME 96 NUMBER 6, pages 645-647| DECEMBER 2014
What do other cardiologists say?
The Q-Symbio study has been received with great interest by cardiologists worldwide. Here are some of the statements that have been made:
Professor Franklin Rosenfeldt, cardiologist, Department of Surgery of Monas University at The Alfred in Prahran, Melbourne, Australia:
Chief Physician, Steen Stender, cardiologist, Gentofte Hospital, Denmark:
Chief Physician, Professor Kristian Thygesen, Institute for Clinical Medicine at Aarhus University and the Dept. of Cardiology at Aarhus University Hospital, Denmark:
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