En esta ocasión le muestro un estudio que demuestra la importancia de la Medicina Ortomolecular en la practica Clinica
Reciente estudio randomizado a doble ciego publicado que confirma que el aporte oral de Coenzima Q 10 disminuye la falla cardiaca y mejora la sobrevida en nuestros pacientes con insuficiencia cardiaca estadio 3-4 de la NYHA. en la practica ortomolecular hace años venimos usando estas dosis de Q 10 en pacientes con este perfil con las consecuentes mejorías clínicas, y en ocasione se había mencionado que la Q 10 apenas se absorbía, y en este caso deja claro que no es tan asi pues estos pacientes en la mayorías eran ancianos que de por si tienen peor condición digestiva dad por su edad y por las patologías de base y sin embargo mejoraron fehacientemente, esto demuestra que la medicina Ortomolecular es importante pues si vamos a las recomendaciones diarias de Q 10 a penas están dispuestas teniendo en cuenta que nuestro organismo es capaz de sintetizarla, lo que pasa es que no siempre en relación con nuestras necesidades y estos son los casos.
La Coenzima Q 10 Actúa potenciando la sintesis energetica a nivel mitocondrial y el miocardiocito es la célula que con mucho presenta mayor densidad mitocondrial, de tal manera que es la mas agradecida a este beneficio, otras célula que suele agradecer este aporte es la neurona y por ende en los pacientes con cuadros demenciales mixtos o en las patologías mitocondriales neurológicas, se convierte en excelente herramienta clínica. Ojo la depleción de Q10 esta relacionada con las patologías hepato renales, el envejecimiento y el uso de estatinas, ademas podríamos utilizar sinergicamente D Ribosa, L Carnitina y Taurina, como ultima herramienta interesante PQQ, y con ellas todos los insuficientes cardiacos mejoran ostensiblemente, la bioquímica lo explica, la clínica ortomolecular aplicada lo evidencia.  Dr Cubrias

Coenzyme Q10 supplementation reduces HF admissions and improves survival: Q-SYMBIO

MAY 31, 2013 

Lisbon, Portugal – In a study bound to be scrutinized when it is finally published, the Q-SYMBIOrandomized, controlled, double-blind clinical trial garnered a fair deal of attention this past week when investigators reported excellent clinical outcomes in chronic heart failure patients treated with coenzyme Q10 (CoQ10).

Metabolic modulation and energetic manipulation in the failing heart is the next frontier of heart-failure management. I want this stuff to work.

Presenting the study at Heart Failure Congress 2013 of the European Society of Cardiology Heart Failure Association, lead investigator Dr Svend Aage Mortensen (Copenhagen University Hospital, Denmark) reported that, at two years, major adverse cardiovascular events (MACE), a composite of unplanned hospitalization due to worsening heart failure, cardiovascular death, and the need for urgent cardiac transplantation and mechanical support, occurred in 14% of patients treated with CoQ10 compared with 25% of patients who received a placebo, a statistically significant difference (p=0.003). All-cause mortality was also significantly lower in the CoQ10-treated patients, with 9% dying compared with 17% in the placebo arm (p=0.01).

In addition to these outcomes, the Q-SYMBIO investigators reported that cardiovascular mortality and admissions for heart failure were significantly lower in those who received CoQ10. In their conclusions, the researchers stated that “CoQ10 should be considered as a part of the maintenance therapy of patients with chronic heart failure.”


Yellow light: Go slow, caution urged

Some, however, considered the recommendations to alter clinical practice on the basis of this 420-patient clinical trial premature. Dr Sanjay Kaul (Cedars-Sinai Medical Center, Los Angeles), for example, said he wants to reserve judgment on the data until they have stood up against the scrutiny of the peer-review process. He noted that the mortality data were first presented at the meeting of the International Coenzyme Q10 Association last November, but these are yet to be published.

“Clinicians should view implausibly large treatment effects observed in small underpowered trials with skepticism, as they are seldom replicated in subsequently conducted large controlled trials,” Kaul toldheartwire. “The examples of vesnarinone in heart failure, [glucose-insulin-potassium] GIK post-STEMI, and perioperative beta-blockers in high-risk vascular surgery quickly come to mind. None of the impressive preliminary results could be replicated. If a finding appears to be ‘too good to be true,’ it usually is.”

One curiosity that also needs to be addressed, added Kaul, is why the Q-SYMBIO trial took more than 10 years to complete. The trial design was first published in 2003. heartwire asked Mortensen to comment on the study and the results, but he declined, saying he wants to wait until after the study is published to discuss the findings.


What other treatments were they taking?

CoQ10 is an antioxidant involved in cellular-energy production. It is postulated that heart-failure patients, who have a measurable deficiency in CoQ10, would benefit from receiving the supplement.

The Q-SYMBIO study included 202 patients randomized to CoQ10 and 218 patients randomized to placebo. All patients included in the study had moderate to severe heart failure (NYHA class 3 or 4) and were receiving “current” pharmacologic therapy. Patients had an average ejection fraction of 31%, and the average age was 62 years. Within three months of treatment, investigators observed a trend toward lower levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP). The clinical improvements in MACE were observed after two years of receiving 100 mg of CoQ10 three times daily compared with those who received the placebo. In addition, 44% of those who received CoQ10 had an improvement in NYHA class compared with 45% of those who received placebo (p=0.047).

To heartwireDr David Kao (University of Denver, Aurora, CO) also said there are some questions that need to be answered before any heart-failure patient should start taking CoQ10 supplements. Specifically, it is not known exactly what “current pharmacologic therapy” entailed for the treated patients. Like Kaul, he would like to see the paper published in order to determine the background regimens, but if it turns out that they were receiving ACE inhibitors/angiotensin-receptor blockers and beta-blockers and CoQ10 still reduced HF admissions and mortality, “that would certainly be a big deal.”

Still, even with all the relevant information, Kao said the trial needs to be replicated in a larger cohort. To substantiate any claims of mortality reduction, the next trial, if Q-SYMBIO stands up once published, would need to include several thousand patients at least.

“I think this is a fascinating area,” Kao told heartwire. “Metabolic modulation and energetic manipulation in the failing heart is the next frontier of heart-failure management. I want this stuff to work. The CoQ10 story has been murky, and there just isn’t quite enough information available on this trial yet to know how to interpret it.”

The study was funded by the International Coenzyme Q10 Association, as well as Kaneka and Pharma Nord, maker of products that contain CoQ10. Kaul and Kao report no conflicts of interest related to the study.