Common Blood Pressure Drugs Tied to Increased Lung Cancer Risk

Angiotensin-converting-enzyme (ACE) inhibitors are associated with increased lung cancer risk compared with angiotensin-receptor blockers (ARBs), an observational study in The BMJ suggests.

Using a U.K. primary care database, researchers identified over 900,000 adults who began treatment with a new antihypertensive drug class from 1995 through 2015. Those with histories of cancer were excluded.

During a mean 6 years' follow-up, lung cancer was diagnosed in 0.8% of the cohort. After adjustment for smoking and other confounders, ACE inhibitor use was associated with significantly increased lung cancer risk relative to ARB use (1.6 vs. 1.2 per 1000 person-years). The increased risk didn't appear until after 5 years of ACE inhibitor use, and then increased with increasing duration of use.

The authors note that ACE inhibitors lead to accumulation of bradykinin in the lungs, which "may directly stimulate growth of lung cancer." An editorialist, meanwhile, concludes, "In an individual patient, concerns about the long term risk of lung cancer should be balanced against gains in life expectancy associated with use of [ACE inhibitors]."

My Take:
ACE inhibitors are one of the three antihypertensive medications I mentioned in last Friday’s blog. Remember that I also mentioned that these drugs cause fluid retention in the lungs and legs (congestive heart failure). Bradykinin is a peptide produced in the kidneys that causes vasodilatation thus lowering blood pressure. When the body is in homeostasis, bradykinin is short lived. However, ACE inhibitors cause this peptide to build up in the lungs, along with the edema, where it acts as a carcinogen.

Congestive Heart Failure

Congestive heart failure is a progressive disease that gets worse over time, especially if it remains untreated. It is often caused by other conditions that weaken the heart, such as heart attack, coronary heart disease, high blood pressure and inflammation or damage to the heart muscle.

A 2016 study estimated that about half of people who develop heart failure live beyond 5 years after being diagnosed. However, there is no simple answer for life expectancy rates, as the average life expectancy for each stage of CHF varies greatly. CHF is not curable, but early detection and treatment may help improve a person’s life expectancy. Following a treatment plan that includes lifestyle changes may help improve their quality of life.

When a person has CHF, their heart has difficulty pumping blood to the other organs in the body. This problem occurs because the walls of the ventricles, which typically pump the blood through the body, become too weak, causing the blood [to] stay in the ventricle, rather than pushing it out. Blood remaining in the heart can cause fluid retention because the heart is not pumping enough blood through the body to push out excess fluids.

CHF has four stages based on the severity of symptoms. Common symptoms include swelling in the legs and feet caused by a buildup of excess fluid, bloating, shortness of breath, fatigue, nausea and chest pain.

Medical treatment for CHF involves reducing the amount of fluid in the body to ease some of the strain on the heart and improving the heart’s ability to pump blood. Doctors may prescribe angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) to help the heart pump blood more effectively. In some cases, doctors may also prescribe beta-blockers to support these efforts and control the heart rate. Doctors also commonly prescribe diuretics for people with CHF, as they may help the body eliminate excess liquid.

Time to Ditch ACE Inhibitors for CVD?

There is “little, if any, clinical reason” to use angiotensin-converting enzyme (ACE) inhibitors for the treatment of hypertension or other cardiovascular indications because angiotensin receptor blockers (ARBs) are just as effective with fewer side effects, a new review concludes.

The review, published in the Journal of the American College of Cardiology on April 3, was led by Franz Messerli, MD, University Hospital, Bern Switzerland.

Messerli and colleagues reviewed data from 119 randomized clinical trials of ACE inhibitors and ARBs in more than half a million patients and found no difference in efficacy between the two drug classes with regard to the surrogate endpoint of blood pressure and the outcomes of all-cause mortality, cardiovascular mortality, myocardial infarction, heart failure, stroke, and end-stage renal disease. But ACE inhibitors have a higher incidence of adverse reaction – namely cough and very low risks of angioedema and fatalities – that are more prevalent in dark-skinned people, they write.

Despite this, most guidelines for the management of patients with cardiovascular disease recommend ACE inhibitors as first-choice therapy, whereas ARBs are merely considered an alternative for ACE inhibitor-intolerant patients, Messerli and colleagues point out.

My Take:
The rest of the article is rebuttal from various cardiologists on the pros and cons of using ARBs in lieu of ACE. The best quote – “And the side effect of angioedema, although rare, can be fatal, and if ACE inhibitors are proposed as part of the polypill then millions will be exposed and fatalities will occur.”

Wisdom Wednesday: Hypertension and Congestive Heart Failure

High blood pressure is an all too common condition as we age. About 29% of Americans have high blood pressure and only half have it under control. By age 55 more than 50% of us suffer from the condition. The health care costs of hypertension are estimated to be in excess of 46 billion dollars a year.

Traditional treatment is medication to reduce the force of the heart contraction. Beta-blockers, calcium channel blockers and ACE inhibitors are commonly used alone or in combination to reduce high blood pressure.

Unfortunately, the most common side effect of these medications is congestive heart failure. Of note, an Internet search for the causes of congestive heart failure will not list medication side effect as a cause.

So you take one or more of these medications to reduce the hypertension but your ankles begin to swell, especially at the end of the day – that’s early congestive heart failure. By reducing the force of the heart contraction, the blood begins to pool in the legs, kidneys, and lungs as pump efficiency drops. Your doctor adds a diuretic to pull off more of the fluid. The swelling goes down but now your legs are cramping or your heart rate becomes erratic from the loss of potassium. So a potassium supplement is added, but that upsets your stomach. A proton-pump inhibitor is next (Nexium or Prilosec) and you’ve reached polypharmacy. Welcome to health care in America.

What is the alternative? Although modern health care considers blood pressure and heart rate as independent variables, the rate, rhythm, and force of the heart contraction are all balanced by input from the brain to the heart. Three of the B vitamins are key players in this complex communication.

Vitamin B1, thiamine is generally stimulatory. I am firmly convinced that the fortification of our grains with thiamine is an ignored factor in both hypertension and heart rhythm disorders like tachycardia and AF (atrial fibrillation).

Lowering Beta-Blocker Dose May Boost Survival After Heart Attack

People treated with low-dose beta blockers after a heart attack may fare better than those given the standard dose of this commonly prescribed medication, a new study shows.

Heart attack patients given just one-fourth of the dosage used in clinical trails lived just as long as patients on a higher dose, according to researchers at Northwestern University in Chicago. And in some cases, those on a low dose lived even longer, with 20-25% increase in survival.

“We set out on a mission to show if you treat patients with the doses that were used in the clinical trials, they will do better. We expected to see patients treated with the lower doses to have worse survival,” lead investigator Dr. Jeffrey Goldberger said in a university news release. “We were shocked to discover that they survived just as well, and possible even better.”

Goldberger is a professor of medicine at Northwestern’s Feinberg School of Medicine and a cardiologist at Northwestern Memorial Hospital. He also directs the cardiac arrhythmia program at Feinberg’s Center for Cardiovascular Innovation.

“We now need to figure out how to dose it in individual patients. That’s something no one has considered in the decades that we have been using this medication,” Goldberger said. “This huge gap in knowledge has been completely unexplored. Since this is the medicine we use in every single heart attack patient, we ought to figure out how to use it properly,” he said in the news release.

Roughly 90% of people treated for a heart attack are given a beta blocker, the study authors noted. This class of medication, which includes metoprolol (Toprol XL) and acebutolol (Sectral), is used to improve survival and prevent further heart attacks.

Wisdom Wednesday: Coenzyme Q-10

Coenzyme Q-10 (CoQ-10) is a very popular supplement. Many people use CoQ-10 for heart conditions, chest pain, diabetes, breast cancer, Parkinson’s disease, muscular dystrophy, chronic fatigue syndrome (CFS), Lyme disease and increasing exercise tolerance.

The chemistry of Co Q-10 is well understood. In the mitochondria of every cell, it facilitates electron transport. This is the process by which energy is transferred from the Krebs’s Citric Acid Cycle (glucose metabolism) to make ATP, the energy molecule of the body. Deficiencies of Co Q-10 impair electron transport severely limiting energy production for all body functions.

Your body produces 75% of the Co Q-10 it needs. The rest comes from the diet. Co Q-10 is found in small amounts in most animal foods. Co Q-10 is a fat and requires other fats in the diet for absorption. So a vegan vegetarian restricting their fat intake might develop a deficiency.

However, the overwhelming cause of Co Q-10 deficiency comes from using statin drugs to lower cholesterol. Drugs like Lipitor inhibit the synthesis of Co Q-10 in the same manner as they inhibit cholesterol synthesis. The symptoms of Co Q-10 deficiency are low energy, fatigue, leg weakness and leg pain. The cardiac myopathy (heart muscle damage) that occurs in 10% of patients taking statin drugs is thought to be a result of Co Q-10 deficiency.