Sudden cardiac death (SCD), also called cardiac arrest, is used to describe a situation in which the heart abruptly and without warning stops working, so no blood can be pumped to the rest of the body. It is responsible for half of all heart disease deaths.
Sudden cardiac death occurs when the heart’s electrical system malfunctions. It is not a heart attack (also known as a myocardial infarcation). A heart attack is when a blockage in a blood vessel interrupts the flow of oxygen-rich blood to the heart, causing heart muscle to die. So if the heart can be compared to a house, SCD occurs when there is an electrical problem and a heart attack – when the problem is the plumbing.Later in that summary it is stated that 75% showed evidence of prior heart attack, and 80% evidence of CVD. So that leaves 25% with no evidence of prior heart attack and 20% with no CVD.
So I do a little math:
* SCD deaths occurring in people with no prior cardiac event that caused discernible damage to heart:
(0.5 of all CD's are SCD's) *( 0.25 no prior heart attack) * 100 = 12.5%
That's one out of every eight.
* SCD deaths occurring in people with no evidence of CVD
(presumably athersclerosis/blockage/etc. but could also include other heart problems):
(0.5 of all CD's are SCD's) *( 0.20 no evidence of CVD) * 100 = 10%
That's one out of every ten.
So why do I care about this? Because the one thing that is most predictive of SCD is elevated free fatty acids (NEFA/FFA), a characteristic of Metabolic Syndrome, Diabetes (Type I & II) ... and VLCD!! While many with pre-diabetes/IR/Type II successfully use carbohydrate restriction to successfully control blood glucose levels, this can be at the expense of further elevation of circulating free fatty acids. A high fat, low carb meal can have the effect on NEFA/FFA levels that a high carb meal would have on blood glucose.
Aims Sudden cardiac death (SCD) is the most common fatal cardiovascular event. Free fatty acids (FFAs) exert several harmful effects on the myocardium and may therefore contribute to SCD. We examined whether fasting FFA predict SCD in patients who had undergone coronary angiography.
Methods and results FFAs were measured at baseline (1997–2000) in 3315 patients scheduled for coronary angiography. Angiographic coronary artery disease was found in 2231 study participants. {My Note: Although this study was in men referred for angiography, roughly 1/3rd were FREE of coronary artery disease}. After a median time of follow-up of 6.85 years, 165 SCD occurred in the entire study population. In a Cox proportional hazards model, the unadjusted hazard ratio (HR) for SCD in the fourth when compared with the first FFA quartile was 2.95 (95% CI 1.84–4.73; P < 0.001). After adjustment for common and emerging cardiovascular risk factors, the HR remained significant at 1.76 (1.03–3.00; P = 0.038). High FFA levels were also significantly associated with all-cause and cardiovascular mortality, even after exclusion of patients with SCD.
Conclusion Our study shows that elevated plasma FFAs are an independent risk factor for future SCD in patients referred to coronary angiography. These results may suggest that modulation of myocardial fatty acid uptake and/or metabolism are a possible target of treatment, but it still remains to be clarified whether high FFA levels are a cause or a consequence of pathological processes that underlie the association between FFA and SCD.
2.
Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population
{My Note: This study separately analyzes a subset of data from the Paris Study where no ischemia was found}
Background— In ischemic conditions, concentration of circulating nonesterified fatty acids (NEFA) is increased and has a proarrhythmic effect that is responsible for ventricular tachyarrhythmias. In nonischemic patients, high NEFA plasma concentration has been shown to be associated with frequent premature ventricular complexes and increased familial risk of cardiovascular disease, but its relation to sudden death has not been studied. We assessed the role of circulating NEFA in sudden death in asymptomatic men in a long-term cohort study.
Methods and Results— A total of 5250 men employed by the city of Paris, aged 42 to 53 in 1967 to 1972, free of known ischemic cardiac disease, and included in the Paris Prospective Study I, completed a second annual examination and had fasting plasma circulating NEFA measured. Each subject underwent a physical examination and ECG, provided blood for laboratory tests, and answered questionnaires administered by trained interviewers. Vital status was obtained for each subject from specific inquiries until he retired; after retirement, it was obtained from death certificates. Body mass index, systolic and diastolic blood pressures, tobacco consumption, parental history of sudden death, fasting cholesterol level, and circulating NEFA concentration were independent factors associated with sudden death during follow up (average, 22 years). When adjusted for confounding factors, circulating NEFA concentration remained an independent risk factor for sudden death (relative risk, 1.70; 95% confidence interval, 1.21 to 2.13) but not for fatal myocardial infarction.
Conclusions— Circulating NEFA concentration is an independent risk factor for sudden death in middle-aged men. Some form of primary prevention could be envisaged in subjects at high risk of sudden death.
These two articles contain a LOT of background in their full texts. A lot of it is disturbing. I won't copy all of it here, but some summaries. If you click on my links to the free full text, you can follow active links to referenced studies, etc.
From #1:
Circulating FFAs are mainly released from triglyceride stores of the adipose tissue and serve as physiologically important energy substrates. An excess of FFA has been implicated in insulin resistance and hepatic steatosis.3,4 Furthermore, elevated FFAs are associated with atherosclerosis5 and hypertension.6 Fatty acid oxidation supplies the heart with ∼70% of its energy but an overwhelming delivery of plasma FFA to the heart, as it is observed in acute coronary syndromes (ACS) and heart failure, may contribute to myocardial dysfunction.2,7,8 High FFA and subsequent increased utilization of fatty acids for energy generation in the ischaemic myocardium may cause a ‘metabolic crisis’ in patients with CAD because fatty acid oxidation requires more oxygen when compared with the use of glucose.2,7 Apart from this, high concentrations of FFA have been shown to exert pro-arrhythmic actions.2,9,10
This study's results: Note 1st Quartile = Fourth of subjects with lowest NEFA on up to the 4th Quartile containing the fourth of subjects with the highest NEFA levels.
I could copy the entire discussion from reference 2, but instead here's a direct link to that section:
http://circ.ahajournals.org/cgi/content/full/104/7/756#SEC3
Why does this concern me? Well, I'm otherwise healthy, but when I ballooned up to the 260's-270's after my first stint on LC, I (not immediately, but when I was that weight for a while) developed a racing heart w/o exertion, listed as a risk factor in my first link. This occurred sometimes in my sleep to the extent that the pounding of my heart in my ears woke me up! After my second stint on LC I had the racing heart with relatively mild exercise -- I was in the low 200's at the time and feeling and looking pretty great at the time (I weigh more than I appear to). Now I had a bunch of tests run that ruled out heart abnormality and wore a Holter monitor and even experienced a related symptom while wearing that. My heart didn't skip any beats, and I've never had an abnormal EKG, but still ... every now and then, even now.
When one looks at fasting lipids, there is always the question of whether it is the circulating lipids themselves that are "causing" something, or if they are merely a symptom of underlying metabolic imbalance, some other factor or factors of which actually cause disease. Fasting triglycerides are an example of this. By now most have seen the differing triglyceride profiles of high carbers vs. low carbers, and excessive carb consumption does lead to elevated fasting trigs. But most of the fat low carbers consume do not exist as trigs, and clearance of triglycerides from the blood has been shown to be faster (this makes sense, we're fat adapted). Still ... is it the triglycerides themselves that exert a directly damaging effect? Or is it that residual trigs indicate a metabolic imbalance? Many of the references for NEFA seem to point to the fact that it is the LEVEL OF THESE IN CIRCULATION that is associated with negative implications or that can elicit a problem in an otherwise healthy animal/human. A HF/VLC diet offers a double assault on NEFA levels. Low insulin (the crown jewel of LC'ers) levels fail to suppress lipolysis, the major source of NEFA, although dietary fats contribute some. I think this is something we should not be so quick to ignore when considering the benefits and risks of carbohydrate restriction.
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