Monthly Archives: December 2020

Statins

Statin – what dat mean Wikipedia?

Statin – what dat mean Wikipedia?

So, THEY want to put me on statins…I want to understand:

  1. what it is?
  2. why am I being herded on to it?
  3. when should I be herded on to it?
  4. how can herding me help me? how can herding me hurt me?
  5. where do I get unprejudiced, non-herding advice on the subject?
  6. who is the best person to inform me going forward without herding?
  7. which, if I’m convinced to take statins should I be herded on to?

When I write THEY, I mean every medical professional I encounter from a diddle-eyed-joe to a damned if I know. There are clinical studies which tout the benefits of statins as great and the side effects as rare. There are observational studies which find that benefits are brought into question and the risk of side effects is significantly higher than the “clinic” counter. Then there are the real life encounters with real herd people (Vern Den Herder) on “the statin”. Their experience with benefit is nil (so far) but their experience with side effects is TOTAL! That being said, I refuse to be SOLD on statins. I prefer, greatly, to be convinced.

Statins are effective in lowering LDL cholesterol. Statins reduce illness and mortality in those who are at high risk of cardiovascular disease. They are used for primary prevention in people at high risk of cardiovascular disease, as well as in secondary prevention for those who have developed cardiovascular disease. Side effects include muscle pain, risk of diabetes and abnormal blood levels of liver enzymes. Also, rare but severe adverse effects, particularly muscle damage. There are various forms of statins. The W.H.O. lists statins as an essential medicine.

In people over the age of 70, statins decrease the risk of cardiovascular disease but ONLY in those with a history of heavy cholesterol blockage in their arteries. Treatment without history of CD reduces events but provides no mortality benefit. Studies overestimate the risk and recommend statins for patients who will not benefit.

Secondary prevention is defined as those having a prior heart attack, stroke, stable or unstable angina, aortic aneurysm, or other arterial ischemic disease, in the presence of atherosclerosis. Patients with vascular diseases reported that simvastatin and pravastatin did not impact cognition. Simvastatin and pravastatin appear to have a reduced incidence of side-effects.

Only a small fraction of side effects reported by people on statins are actually attributable to the statin according to review. Evidence does not support an association between statin use and cognitive decline. The FDA includes a warning about the potential for non-serious and reversible cognitive side effects with the medication (memory loss, confusion).

In observational studies 10–15% of people who take statins experience muscle problems (pain), much higher than those seen in randomized clinical trials. CoQ10 supplements are sometimes used to treat statin-associated myopathy. Myopathy risk was over 10-fold greater if cerivastatin was used, or if the standard statins were combined with a fibrate. Lovastatin promotes muscle fiber damage.

Oh, yeah, here’s one for you: Studies have found that the use of statins may protect against getting osteoporosis and fractures OR may lead to getting osteoporosis and fractures. Dosage, THEY say, is the key.

Natural statins are produced by fungi. Most circulating cholesterol comes from internal manufacture rather than the diet. Liver cells sense the reduced levels of liver cholesterol and seek to compensate by synthesizing LDL receptors to draw cholesterol out of the circulation. Oh, I forgot to mention, this is a known fact but in reference to rabbits.

Inhibiting of lipids binding to protein molecules results in a number of unwanted side effects associated with statins. The multiple effects of statins remain controversial. Statins are divided into two groups which are fermentation derived and synthetic. Natural statins occur in foods such as oyster mushrooms and red yeast rice. The first statin agent was mevastatin produced by penicillium. As of 2016 misleading claims exaggerating the adverse effects of statins had received widespread media coverage, with a consequent negative impact to public health

So, how did I do? Did I get answers to all of my questions…let’s see:

  1. what it is? Statins are effective in lowering LDL cholesterol.
  2. why am I being herded on to it? Secondary prevention for…aortic aneurysm.
  3. when should I be herded on to it? AAA
  4. how can herding me help me? how can herding me hurt me?

Help=if prevents rupture.

Hurt=muscle pain or damage, diabetes, abnormal blood levels, memory loss

  1. where do I get unprejudiced, non-herding advice on the subject?

Critical studies not pharmaceutical company related

  1. who is the best person to inform me going forward without herding?

Non-involved doctor or scientist, non-cardiologist

  1. which, if I’m convinced to take statins should I be herded on to? Simvastatin and pravastatin
Conditions

Abdominal aortic aneurysm – what dat mean Wikipedia?

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Abdominal aortic aneurysm – what dat mean Wikipedia?

So, I have a triple A (AAA) = abdominal aortic aneurysm.

I want to understand:

  1. what it is,
  2. why I have it,
  3. when it becomes dangerous,
  4. how it can be fixed,
  5. where the fix is in my body, and…and…
  6. who gonna do it.

My first stop was my third cardiologist. I say third because my first cardi be tryin’ to frightin’ me into surgery. Oh, you have dangerous cholesterol levels (210). Oh, you need an immediate EKG, stress test, CT scan. Oh, you had a heart attack (shadow on the film). Second cardi be sayin’ don’t you be eatin them dead animals. Eat statins. I do. Why are you here? Where is your scan. Oh, your AAA got bigger. No biggy. Back to the third. Third cardi be sayin’ your second cardi say you havin’ all dem 140 BPs (a single instance). Statins, plaque, AAA, oh my!

AAA is enlargement of abdominal aorta to 3 cm (1.2 inches) or greater. Typically found in men over 50 who smoke. Prevention in non-smokers include treating high: blood pressure, cholesterol and weight. Surgery recommended when AAA grows to > 5.5 cm. Repair may be open surgery or EVAR. The procedure involves the placement of an expandable stent graft within the aorta to treat aortic disease without operating directly on the aorta. Risk of rupture when less than 5.5 cm is below 1% in next year.

EVAR procedure: The procedure can be performed under general, regional (spinal or epidural) or even local anesthesia. Access to the patient’s femoral arteries can be with surgical incisions or percutaneously in the groin on both sides. Vascular sheaths are introduced into the patient’s femoral arteries, through which guidewires, catheters and the endograft are passed.

Without being a smoker, genetics is the most likely explanation for a AAA. High blood pressure contributes to AAA progression. CT scan has 100% success detecting AAA. A rupture occurs when mechanical stress (peak wall stress, PWS) exceeds wall strength (peak wall rupture risk, PWRR). PWS/PWRR are more reliable than diameter in assessing rupture risk.

A diameter between 3 and 5 cm is classified as moderate. For s non-smoker the only prevention mentioned is hypertension treatment. A repeat ultrasound should be repeated every three years for diameters between 3 and 3.9. Intervention when growth is more than 1 cm/year or diameter bigger than 5.5 cm. Medication includes BP and lipid. Repair prior to 5.5 cm is not supported by evidence. EVAR has the benefit of lowering aneurysm related mortality.

A AAA under 4 cm with a growth rate of 0.39 cm/yr has a rupture risk of zero. If over 3.9 but under 5, 0.5-5%. Rupture risk accuracy improves with both PWS/PWRR. The post-operative mortality rate is 1-6% for AAA repaired before rupture.

A biomechanics based approach may be more suitable than current diameter approach. Tortuous anatomies are more complex. Protection against AAA in mice has been discovered in the lab. Another mice study showed that progression and survival can be improved with targeted treatment.

Did I accomplish my stated goals from my first paragraph? Let’s look.

  1. What is it?: AAA is enlargement of abdominal aorta to 3 cm (1.2 inches) or greater.
  2. Why is it?: I’m over 50 and may have high blood pressure (not), cholesterol (some), overweight (slightly).
  3. When is treatment? When diameter exceeds 5.5 cm and PWS exceeds PWRR.
  4. How is treatment administered? Place an expandable stent within the aorta (EVAR).
  5. Where the fix is? Under anesthesia, through the femoral artery
  6. Who gonna do it? Cardiologist who treats AAA > 5.5 cm with EVAR after using both diameter and biomechanical assessment.

By Jove, I think we’ve got it.