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They have treated heart disease for 40 years, but it now seems that beta blockers don’t work. What went wrong?
IT IS very rare for new evidence to question or even negate the utility of a well-established class of drugs. But after four decades as a standard therapy for heart disease and high blood pressure, it looks like this fate will befall beta blockers. Two major studies published within about a week of each other suggest that the drugs do not work for these conditions.
The beta blocker drug used to treat heart diseases such as managing irregular heartbeat, treatment of hypertension and protection of the heart after a cardiac arrest...
While the result held for the standard classes of heart drugs - statins, anticoagulants and antihypertensives - it did not for beta blockers. Regardless of whether or not patients stuck to their regimen, their risk of dying was the same. Taken together with the JAMA study, it becomes very reasonable to question the benefit of beta blockers for treating these conditions.
What comes next is impossible to predict, but we may well be seeing a rare case of medical wisdom being overturned almost overnight. Beta blockers are not dangerous and have been in use for such a long time that it is unlikely that we will see an immediate cessation. But these results are hard to ignore, and cardiologists will be paying careful attention.
Adverse drug reactions (ADRs) associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema. Due to the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other, less lipophilic, beta blockers to cause sleep disturbances, such as insomnia and vivid dreams and nightmares.
Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-selective (often termed "cardioselective") agents, however receptor selectivity diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at the macula densa, inhibits renin release, thus decreasing the release of aldosterone. This causes hyponatremia and hyperkalemia.
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate hepatic glycogen breakdown (glycogenolysis) and pancreatic release of glucagon, which work together to increase plasma glucose. Therefore, blocking β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic side effects in diabetic patients; however, the tachycardia which serves as a warning sign for insulin-induced hypoglycemia may be masked. Therefore, beta blockers are to be used cautiously in diabetics. 
A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developing diabetes, while ACE inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers) actually decrease the risk of diabetes. Clinical guidelines in Great Britain, but not in the United States, call for avoiding diuretics and beta blockers as first-line treatment of hypertension due to the risk of diabetes.
Beta blockers must not be used in the treatment of coc aine, amphetamine, or other alpha-adrenergic stimulant overdose. The blockade of only beta receptors increases hypertension, reduces coronary blood flow, left ventricular function, and cardiac output and tissue perfusion by means of leaving the alpha-adrenergic system stimulation unopposed. The appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant abuse are vasodilators such as nitroglycerin, diuretics such as furosemide and alpha blockers such as phentolamine.
Which raises the question: why has it taken so long to find out? It is worth noting at this point that this is not yet another case of a drug entering the market only to be withdrawn later because of lack of efficacy or even adverse reactions which could have been noticed with longer or larger trials. It is simply a new medical revelation. The authors of the JAMA paper provide a reasonable explanation of the conflict between their results and earlier studies.
Damaged hearts are more prone to fatal irregular beats, and beta blockers are useful in controlling this. But with the advent of reperfusion therapy, people who survived heart attacks suffered less cardiac damage, so the frequency of fatal arrhythmias was lower. Put simply, the beta blocker effect was significant before the advent of this improved treatment, but the beneficial effect has since disappeared.
The key word is "earlier". Most clinical trials on beta blockers took place before reperfusion therapy became standard treatment following heart attacks. Reperfusion involves opening the blocked artery by surgery or pharmaceuticals, and has been shown to significantly reduce damage to the heart.
But with the advent of reperfusion therapy, people who survived heart attacks suffered less cardiac damage, so the frequency of fatal arrhythmias was lower.
Put simply, the beta blocker effect was significant before the advent of this improved treatment, but the beneficial effect has since disappeared.
Originally posted by marg6043
I had a doctor that push on me a beta blocker until I gave up and took it, I never had depression before in my life until I took this drug to make things short, it was the worst side effects ever coming from a prescribe drug and I had my fair share of them
BTW it actually increased my blood pressure because the anxiety I developed.
You can not get off of them easily as they can cause a rebound effect and give you an actually hart attack.
Conclusion In this observational study of patients with either CAD risk factors only, known prior MI, or known CAD without MI, the use of β-blockers was not associated with a lower risk of composite cardiovascular events.