Serum cholesterol, statins and heart failure

Is there a relationship between serum cholesterol level and prognosis following heart failure? Does lipid lowering have any effect on survival following CCF? I have posted earlier that the use of statins seems to improve the prognosis of CCF.

In the just ended AHA Annual Scientific Session in Chicago, Dr Periaswamy Velavan and investigators of Hull, UK, presented their work on the 12 weeks mortality of >5,000 patients with heart failure. True, this is very much a registry study and not a controlled trial. However, it does give important pointers regarding the relationhip of serum cholesterol and CCF survival.
In summary, they concluded from their study that too high a cholesterol (>200mg/dl), or too low (<150mg/dl) a cholesterol, was associated with poorer CCF prognosis. The relationship of serum cholesterol and heart failure survival, seemed to be U-shape. The other important fact that they reported was that the use of statins seemed to improve prognosis. How then do you reconcile these two findings?

It would seem that, like everything in nature, we must always do things in moderation. Too low or too high (the extremes) a cholesterol is bad. Taking statins may help improve prognosis of CCF but avoid high doses of powerful statins. Something moderate will do. As I noted in my last posting on this subject, there seem to be some anti-inflammatory effects of statins on the inflammatory component of CCF.

Athelete's heart or early CAD

Is there such a thing as the athletes' heart? I am encouraging my patients to exercise as a means of primary protection against coronary heart disease. Some of my patients are quite serious about exercise and in fact are runing regularly with the hash harriers and pacemaker clubs. In fact a few of them are running 40 Km marathons regularly. Is this wise?

When we see "fit" well trained patients with a low heart rate and enlarged heart, we attribute all this to their fitness and regular exercise. The enlarged heart we call "athlete's heart". But is there such an entity and is it normal. We have written earlier, that marathon running can be associated with rises in CKMB and troponin T, suggesting myo-sacomere destruction with marathon running.

At the recent AHA annual scientific meeting in Chicago, Dt Stephan Mohlenkamp presented the Master Marathon Study. They studied about 100 marathon runners (run at least 20 marathons over the last 20 years), who had a low cardiac risk profile using the Framingham Scores. They subjected these runners to echocardiograms, the MSCT and the Calcium score, and found that many of them had enlarged heart with increase calcium score, suggesting that these marathon runners in fact may have subclinical CAD.

A week later, at the American Radiological Society Annual Scientific meeting, also held in Chicago, Dr Torleif Sandner of Munich also presented another study done in on the same population of now 110 marathon runners, now average years 57, to MRI scans of the heart in an attempt to measure their LV mass. They found that these marathon runners all had an increase LV mass of 150 grams or more. Obviously this second study was done in collaboration with the first study. When they compared their studies, they found that those runners with higher calcium score also had higher LV mass, suggesting that the increase LV mass may be related to early CAD as suggested by the increase calcium score. Interesting.

I have never been a firm believer in calcium score having a positive correlation with presence of CAD. I have always thought that zero calcium score is better correlated with lack of CAD. Anyway, I thought it interesting that fit marathon runners should be careful. You may have early CAD. If that is true, it further supports the earlier posting that the rise in CKMB and Troponin T may be due to some degree of heart muscle damage from micro-infarcts. Marathon runners beware.

Watch that temper. Sudden cardiac death

One of the common cause of cardiac death is sudden cardiac death (SCD), defined as death within 24hrs of developing symptoms. These are the deaths reported as sudden collapses in golf courses, while driving, while having sex, people found slumped in cars (if no foul play suspected). In some ways, especially for senior citizens, such a mode of death if what we all wish for. No suffering. Just go suddenly and peacefully.

Medical science has spent much time and effort studying this phenomenon, obviously so that we can find a way of preventing them and treating them. We needed to know the triggers of SCD. Remember, there was a time when scientists (including one of our own Malaysian - Dr Reggis de Silva), were studying the Voodoo behaviour and how it cause people to collapse and die suddenly. How does Voodoo kill?

Well, we do know that patients with poor heart systolic function, are prone to sudden cardiac death. These are the patients who receive antomatic implantable cardiac defibrillator (AICD). These are pacemakers implanted in the heart, that can detect ventricular tachycardia or fibrillation, and deliver a program defib. shock to terminate the arrhythmia.

The just ended AHA annual scientific meeting in Chicago had a paper presented from Harvard, Boston, which studied the triggers for ventricular fibrillation. The investigators studied the records of people with AICD and asked them to record the episodes of defib shocks and recall the events before the shocks (you see the patient can feel the shocks and they hated it. So they are motivated to assist in studies that can help them prevent the need for the shocks). There were 1188 patients under study, and during the period under study, there were 199 episodes of defib. The patients with severe anger and fury had a 16 fold increase in defibs. suggeting that severe anger or anger was an important trigger for Vent. Fib. To be honest, these are patients with poor LV systolic function. Does it apply to us. I am sure that there is some relationship with increase sympathetic tone and Vent.Fib. So the next time you lose your head, be aware, it may stop your heart too.