Coronary vasospasm culminating in thromboels and infarction following “successful” coronary angioplasty

Klevan, Thomas; Deckelbaum, Lawrence I.; Wohlgelernter, Daniel; Cleman, Michael

doi:10.1016/0002-8703(87)90937-9

Cited by 17 publications

(17 citation statements)

References 5 publications

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“…believe that it is due to sympathetic denervation during the surgery that would eliminate the ischemia mediated reflex coronary spasm [83][84][85][86]88 as well as reduce norepinephrine release, thereby reducing wasteful O 2 consumption at adrenergic nerve terminals, which would also reduce coronary reflex spasm, platelet aggregation, and thrombus formation, all of which are facilitated by catecholamines. [126][127][128][129][130] From looking at the collateral vascular development (Fig. 4b) in Fulton's 131 injection study, it is hard to imagine how coronary bypass surgery could possibly improve the generation of useful alternate vascular pathways to the myocardium that have not already been created by natural collateral development in response to chronic ischemia.…”

Section: Myofibrillar Degeneration 89-91mentioning

confidence: 99%

“…10,151 Such stresses, which are controlled by interactions with higher centers, are critical factors in causing myocardial IsHD, arrhythmias, and SCD and very likely contribute to occlusive spasm and atherosclerotic obstructive coronary disease as well as thrombus formation. 3,9,13,15,74,79,[125][126][127][128][129][130] Indeed, anger alone has been shown to cause severe coronary artery spasm 54 and trigger arrhythmias. 81,82 Other strong emotions have also been claimed to be a frequent precursor of therapeutic ICD discharge in recent studies.…”

Section: The Concept Of Metabolic Neurohormonal Cardiovascular Diseasementioning

confidence: 99%

“…2,10,74,79 This evidence has been obscured and ignored because the usual parallel occurrence of CAD together with IsHD has been widely, but mistakenly, interpreted as a putative cause-and-effect relationship, particularly enshrined when occluding thrombus is present, 74 which may itself be enhanced as a consequence of adrenergic actions causing coronary spasm and platelet aggregation. 15,20,25,26,47,55,[126][127][128][129] which traps platelet aggregates that facilitate thrombus formation. [125][126][127][128][129] Catecholamines 125 and ADP accumulation during ischemia 126 both facilitate platelet aggregation, abnormal coronary reflex dynamics, and coronary vasospasm by releasing vasospastic substances, which further facilitates uptake of thrombin by platelets leading to thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

“…15,20,25,26,47,55,[126][127][128][129] which traps platelet aggregates that facilitate thrombus formation. [125][126][127][128][129] Catecholamines 125 and ADP accumulation during ischemia 126 both facilitate platelet aggregation, abnormal coronary reflex dynamics, and coronary vasospasm by releasing vasospastic substances, which further facilitates uptake of thrombin by platelets leading to thrombus formation. 74,[117][118][119][120][121][122][123][124][125][126][127][128][129][130] Most importantly, it is not commonly appreciated that catecholamines often cause an excessive increase in wasteful O 2 consumption, 3,4,[7][8][9][10][11] which can be blocked by sympathetic denervation 69 or pharmacologic adrenergic blockade (as shown in clinical study), and most effectively by down-regulation of the sympathetic nervous system by exercise, 10,11 which substantially increases cardiac efficiency and lowers myocardial O 2 consumption for any situation.…”

Section: Introductionmentioning

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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Section: Myofibrillar Degeneration 89-91mentioning

confidence: 99%

Section: The Concept Of Metabolic Neurohormonal Cardiovascular Diseasementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…These factors may all play a role in acute occlusion in the period immediately after angioplasty. [7][8][9][10] The propensity to develop spasm may not be limited to the period very early after angioplasty.11-13 Quyyumi et al,12 using an ergonovine (ERGO) infusion, produced coronary spasm at the site of angioplasty in five of 14 patients between 6 and 20 weeks after angioplasty. The relation between provoked spasm and restenosis in patients undergoing coronary angioplasty was studied by Bertrand et al 13 The presence of ERGO-induced coronary spasm at 6 months was associated with a higher incidence of restenosis.…”

mentioning

confidence: 99%

Vascular reactivity after balloon angioplasty in an atherosclerotic rabbit.

et al. 1990

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Alterations in vessel wall reactivity (VR) at or adjacent to the dilation site after balloon angioplasty (BA) may vary according to the inflation protocol and the time after angioplasty and may influence outcome. In 64 atherosclerotic rabbit femoral arteries, we evaluated VR after BA with intravenous ergonovine (ERGO) (40 ,ug/min for 5 minutes) and intra-arterial nitroglycerin (NTG) (2,500 ,ug single bolus)

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Coronary artery spasm culminating in thrombosis following ergonovine stimulation

et al. 1993

Cathet. Cardiovasc. Diagn.

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A 53-yr-old active man with angina but no angiographically significant obstructive coronary artery disease developed refractory spasm following ergonovine provocation. This resulted in thrombus formation and myocardial infarction. As such, this is the first case in which thrombosis developed at the site of intense coronary artery spasm induced by ergonovine, all of which were documented angiographically. Despite the notable safety of this test, this case re-emphasizes the potential of ergonovine to produce intractable myocardial ischemia and infarction.

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Coronary vasospasm culminating in thromboels and infarction following “successful” coronary angioplasty

Cited by 17 publications

References 5 publications

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

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

Vascular reactivity after balloon angioplasty in an atherosclerotic rabbit.

Coronary artery spasm culminating in thrombosis following ergonovine stimulation

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