One of the first symptoms of a pet’s failing heart is a tendency to retain fluid. At the first sign of heart disease, particularly congestive heart failure, your vet is likely to prescribe a ‘water pill.’ These drugs force the kidneys to excrete more fluid than usual, and are also used to remove fluid from the lungs.
In dogs and cats (and humans), diuretics work by interfering with the kidney’s filtration system. The job of the kidneys is to control the amount of fluid and electrolytes
in the blood by filtering out water, waste products, and salts such as sodium and potassium from what should be reabsorbed back into the bloodstream. By excreting some of the body’s fluid as urine, the kidneys reduce blood volume and, thus, the load on the heart.
The usual first line of treatment for dogs and cats is furosemide (frusemide, or Lasix)(Aust Vet J, 1995; 72: 401-3). This is a ‘loop’ diuretic that eliminates excess fluid from the bloodstream by affecting the transport of sodium so that the kidneys absorb less water.
Most vets fail to appreciate the devastating effect these drugs can have on the kidneys. Furosemide activates the hormonal renin- angiotensin-aldosterone system (RAAS) that regulates blood pressure and fluid balance. When an animal’s blood volume is low, certain cells in the kidneys secrete a substance that makes angiotensin, a peptide that causes blood vessels to constrict, thus raising blood pressure and stimulating the secretion of the hormone aldosterone, which causes the kidneys to re-absorb more fluid. As a consequence, the long-term effect of the diuretic is to undo its own best efforts by signaling that it’s time to crank up fluid uptake.
In one recent study, furosemide was linked to a threefold increase in RAAS activity in dogs, especially when combined with pimobendan (Vetmedin) (J Vet Intern Med, 2009; 23: 673-786). The authors concluded that “furosemide is not recom-mended for chronic use in the absence of concurrent therapy to blunt RAAS activity”. In other words, furosemide should only be used if you throw in a second drug, such as an ACE inhibitor, to counteract its side-effects.
Diuretics cause other serious side-effects, such as excessive dehydration and thirst, muscle weak-ness, dizziness and hypokalaemia (too-low potassium). Also, diuretics interact with other common drugs given to animals with heart conditions or high blood pressure, particularly digoxin.
These effects lead vets to turn to potassium-sparing diuretics, such as spironolactone, or to use them in combination with other heart drugs and diuretics. One double-blind study of dogs given an ACE inhibitor, furosemide and digoxin (if needed), and either spironolactone or a placebo, showed that spironolactone slowed the progression of disease and increased survival time (J Vet Intern Med, 2010; 24: 331-41).
Yet, in another study, when added to the usual cocktail of ACE inhibitor, furosemide, pimobendan and digoxin, spironolactone had no effect on survival time (J Vet Pharmacol Ther, 2011; 34: 322-31).
By sparing potassium, spironolactone can often raise potassium to excessive and even life-threateningly high levels, especially when given with an ACE inhibitor. So, as with furosemide, it’s important to have your pet’s potassium levels monitored regularly when using this drug.
Vets often try to counter the ill effects of diuretics by tossing in an ACE inhibitor (enalapril: Enacard, Vasotec; benazepril: Lotensin, Fortekor) to relax blood vessels, thus lowering blood pressure, and increasing blood flow to the heart by blocking the angiotensin-converting enzyme (ACE) that makes an agent that constricts the blood vessels.
However, enalaril, initially hailed as a boost to survival, albeit ‘modestly’ (J Am Vet Med Assoc, 2007; 231: 1061-9), has proved in follow-up studies of certain breeds to have no such advantage (J Vet Intern Med, 2002; 16: 80-8).
Yet, these drugs, often given to prevent renal damage, wreak havoc on the kidneys and liver. In fact, ACE inhibitors contribute to severe renal insufficiency. If an animal is also on a salt-restricted diet, these drugs, like diuretics, activate the RAAS system, again undermining the basis for giving the drug in the first place.
ACE inhibitors also damage other vital organs, particularly the liver by accumulating toxins, along with nausea or vomiting, loss of appetite and a dry cough-all symptoms that usually prompt the vet to reach for his pen and pad.
The only truly promising therapy from conventional medicine may be costly heart surgery to repair or replace failing valves, using tissue from pigs or cows; this claims to have a 70-per-cent cure rate among animals that manage to survive the surgery and the risk of rejection of foreign tissue.
Nevertheless, vets continue to experiment with a cocktail of human heart drugs on their pet cardiac patients in the hopes of staying one step ahead of the side-effects that are alarmingly similar to the disease itself. Although some animals do stabilize with these drugs, the health benefits are often modest, and often with a decreased quality of life; too often, they’re also a fast-track to euthanasia.
Lynne McTaggart
Factfile: Natural heart-drug alternatives
If you prefer not to experiment with drug combos on your pet, you could try some natural approaches. Start as soon as your animal is diagnosed.
WDDTY ISSUE 22 NO.9, NOV. 2011
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