The body’s stress response system is a powerful chain reaction of enzymes, proteins, and neurotransmitters, enabling it to respond to emergencies or danger. Renin (from the kidney) changes angiotensinogen (from the liver) into a protein, angiotensin 1. Angiotensin converting enzyme (from the lungs) changes the protein into angiotensin 2 which causes blood vessels to contract and speeds the heart rate. But what benefits the body in a crisis can harm it in the long run.
A steady supply of angiotensin 2 leads to high blood pressure (hypertension). In the 1960s, ACE inhibitors were developed to prevent the formation of angiotensin 2. It causes the heart rate to slow and blood vessels to relax, enabling blood to safely flow through the body. This removes unnecessary stress from the heart and kidneys, allowing them to function as they should.
Side effects are common among all drug classes. Common to ACEIs are swelling of tissue below the skin (angioedema) and a dry cough. ACE inhibitor cough occurs in less than 20 percent of those taking ACEIs, primarily blacks and women. Nitric oxide, anti-inflammatories, iron, and other treatments may be used to treat ACEI cough. Although not effective for all sufferers, a switch to another drug class, angiotensin receptor blocker (ARB), has been beneficial for many. It has the added advantage of providing protection for the kidneys.
The second-most common side effect of taking an ACEI is a swelling of tissue below the skin, mostly the tongue, throat, lips, and cheeks. The swelling could become severe enough to close the throat. Adequate time to monitor and treat the swelling is possible in general because the swelling occurs over a period of hours. A previous episode of angioedema and race (black), are the two largest risk factors; smoking, gender (women), and increased age are lesser ones. Diabetics taking a drug class called gliptins are also at risk. A person can go many years before experiencing this problem; it has often been mistaken for an allergic reaction to food. However, with increased awareness, doctors are more likely to make the connection between the two. The current wisdom is to switch to something else – most likely an ARB – for blood pressure management.
The way ACEI affects a compound that also relaxes blood vessels, bradykinin, seems to be the common factor in ACEI cough and angioedema. While a new drug class is being readied to address that interference, sufferers are best served now by being informed patients. Effective communication between patient and physician is critical to properly identifying and treating ACE inhibitor cough and angioedema. The result is a cough-free, edema-free patient who manages their health well.
- Monopril (fosinopril)
- Capoten (captopril)
- Altace (ramipril)
- Univasc (moexipril)
- Prinivil, Zestril (lisinopril)
- Accupril (quinapril)
- Vasotec (enalapril)
- Mavik (trandolapril)
- Lotensin (benazepril)
- Aceon (perindopril)
May be combined with thiazides, drugs that increase urination (diuretics).
- Uniretic (hydrochlorothiazide/moexipril)
- Zestoretic (hydrochlorothiazide/lisinopril)
- Accuretic (hydrochlorothiazide/quinapril)
- Prinzide (hydrochlorothiazide/lisinopril)
- Capozide (captopril/hydrochlorothiazide)
- Lotensin HCT (benazepril/hydrochlorothiazide)
- Monopril HCT (fosinopril/hydrochlorothiazide)
- Quinaretic (hydrochlorothiazide/quinapril)
- Vaseretic (enalapril/hydrochlorothiazide)
They can also be combined with calcium channel blockers, a drug class that keeps the heart from working too hard and blood vessels from contracting by reducing absorption of calcium.
- Tarka (trandolapril/verapamil)
- Teczem (diltiazem/enalapril)
- Amlobenz or Lotrel (amlodipine/benazepril)
- Lexxel (enalapril/felodipine)
- Teveten (eprosartan)
- Benicar (olmesartan)
- Edarbi (azilsartan medoxomil)
- Micardis (telmisartan)
- Cozaar (losartan)
- Diovan (valsartan)
- Atacand (candesartan)
- Avapro (irbesartan)