Acute myocardial infarction in post infarct patient possibly through beta blocker-induced coronary artery spasm

Nanas, John N.; Sutton, Richard; Alazraki, Naomi P.; Tsagaris, Theofilos J.

doi:10.1016/0002-8703(87)90284-5

Cited by 11 publications

(10 citation statements)

References 16 publications

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“…Eighteen patients (9.8%) died after myocardial infarction. Age was not related to myocardial (15) Nifedipine (9), diltiazem (4), verapamil (2) ACE inhibitors (6) Captopril (1), lisinopril (2), perindopril (2), enalapril (1) b-adrenoceptor blockers (5) Oxprenolol (1), pindolol (1), atenolol (1), metoprolol (2) a 1 -adrenoceptor blockers (2) Urapidil (1), prazosin (1) Other (9) Diuretics (7), ibopamine (1), disopyramide (1) Central nervous system (53) Antidepressants (17) Imipramine (1), amitriptyline (2), mianserin (1), moclobemide (4), uvoxamine (2), trazodone (2),¯uoxetine (3), maprotiline (1), doxepine (1) Antipsychotics (1) Clozapine (1) Anti-migraine (35) Ergotamine (1), sumatriptan (33), methysergide (1) Respiratory system (15) b-sympatho-mimetics (7) Salbutamol (3), salmeterol (4), formoterol (2) Antihistamines (5) Terfenadine (1), cetirizine (2), cinnarizine (2) Other (3)…”

Section: Resultsmentioning

confidence: 99%

Drug-induced chest pain and myocardial infarction. Reports to a national centre and review of the literature

Ottervanger¹,

Wilson²,

Stricker³

1997

European Journal of Clinical Pharmacology

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Section: Resultsmentioning

confidence: 99%

Drug-induced chest pain and myocardial infarction. Reports to a national centre and review of the literature

Ottervanger¹,

Wilson²,

Stricker³

1997

European Journal of Clinical Pharmacology

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“…71,94,95,[133][134][135] Paradoxically, ␤-blockade alone may elicit coronary spasm by enhancing alphaconstrictor receptor excitation 71,94,95 and by blocking the physiological ␤-dilator response. In fact, ␤-blockade per se was reported to have caused a new AMI in a post-AMI patient who it was supposed to protect, 95 probably by inducing coronary spasm by amplifying alpha-adrenergic overload stimulation. 71 For analogy, it is like closing 1 hole in a leaky pot with 2 holes; the buildup of water causes a faster leakage through the hole that remains open.…”

Section: Connecting the Dots Leading To The Concept Of Adcvhd And Neumentioning

confidence: 99%

“…138 Our data suggest that total blockade of norepinephrine release at the nerve terminals will provide better sympathetic blockade than ␤-receptor blockade alone. 71,94,95,136,137 In fact, ␤-receptor blockade may actually enhance alpha constrictor action, 94,95 something that bretylium would also block if they were given together, which is the ideal therapy in my (M.B.) view.…”

Section: Connecting the Dots Leading To The Concept Of Adcvhd And Neumentioning

confidence: 99%

“…87,155,203 Moreover, ␤-receptor blockade may cause coronary vasoconstriction by blocking ␤-adrenergic action, which is a physiological mechanism to induce coronary vasodilatation. 94,95 It may also enhance alpha-adrenergic vasoconstrictor action. 71,94 As shown in Figure 3, bretylium given together with ␤-receptor blockers (particularly propranolol) provides a significantly more comprehensive and therapeutic antifibrillatory, antiarrhythmic, and antiadrenergic action on the myocardium than bretylium alone.…”

Section: New and Better Bretylium Formulationmentioning

confidence: 99%

“…Moreover, bretylium reduces coronary resistance 214 in contrast to ␤-blockade alone, which may increase coronary resistance. 94,95 This would be a completely safe intervention for immediate self-administration in vulnerable patients as long as the patient remains supine until getting physician treatment or until tolerance to the orthostatic hypotension develops or is reversed with protriptyline. 220 The risk-free benefits of preventing VF and aborting the progression of a possible AMI is much more rational, safe, and achievable with bretylium than with total body cooling, as recently advocated by the AHA to protect the brain.…”

Section: New and Better Bretylium Formulationmentioning

confidence: 99%

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Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholestero...

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Syncope and recurrent long sinus arrest in vasospastic angina

Hasegawa

Kitamura

Mashiba

1992

Cardiovasc Drug Ther

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Acute myocardial infarction in post infarct patient possibly through beta blocker-induced coronary artery spasm

Cited by 11 publications

References 16 publications

Drug-induced chest pain and myocardial infarction. Reports to a national centre and review of the literature

Drug-induced chest pain and myocardial infarction. Reports to a national centre and review of the literature

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Syncope and recurrent long sinus arrest in vasospastic angina

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