Role Of Coronary Artery Spasm Research Articles

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data.

Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41-50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn't been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type channel blockers result in the long-term improvement of coronary blood flow in patients with MVO.

Association of the interleukine-6 polymorphism with catheter-induced coronary artery spasm in Egyptians.

The role of coronary artery spasm (CAS) was extended beyond variant angina to ischemic heart disease in general, including effort angina, unstable angina, acute myocardial infarction (MI) and sudden death. It is difficult and cumbersome to examine CAS during coronary angiography. Risk factors for CAS include smoking and genetic polymorphisms. We aimed to investigate the association of the interleukin-6 (IL-6) polymorphism with catheter-induced CAS in Egyptian patients who undergo coronary angiography. This is a case-control study. Two hundred patients with chronic coronary artery disease who underwent elective coronary angiography were included in the study. Patients were divided into two groups: the non-CAS group (100 patients) and the CAS group (100 patients). The subjects were genotyped to the -572 C>G (rs 1800796) polymorphism of the IL-6 gene by PCR-restriction fragment length polymorphism. We found that patients with CAS have more risk factors for atherosclerosis compared to those without CAS. Smoking, the IL-6 GG genotype, and the G allele were independent risk factors for CAS. We concluded that the GG genotype and G allele of the IL-6 gene are associated with CAS. Smoking, the GG genotype, and the G allele of the IL-6 gene are independent predictors of catheter-induced CAS.

Downregulated caveolin-1 expression serves a potential role in coronary artery spasm by inducing nitric oxide production in vitro.

The present study aimed to investigate the effects of downregulated caveolin-1 (Cav-1) expression on nitric oxide (NO) production in lipopolysaccharide (LPS)-damaged primary human umbilical vein endothelial cells (HUVECs) in a model of coronary artery spasm (CAS) microenvironment induced by acetylcholine (ACh) treatment. Small interfering RNA (siRNA)-mediated Cav-1 downregulation in HUVECs was confirmed by western blotting. The cell viability and superoxide dismutase (SOD) inhibition in HUVECs incubated with LPS (0, 10, 25, 50, 75 and 100 µg/ml) were measured by cell counting kit-8 assay and a SOD kit, respectively. Intracellular Ca2+ [(Ca2+)i] in Fluo4-acetoxymethyl ester-loaded cells was detected by fluorescence microscopy. NO levels in the cell culture supernatants were measured by the nitrate reductase method. The results indicated that transfection with Cav-1 siRNA, in particular siCav-1 (2), downregulated the Cav-1 protein expression. LPS at a dose of 75 µg/ml induced a significant decrease in HUVECs/si-NC and HUVECs/siCav-1 viability compared with the other concentrations of LPS. Compared with the effects of untreated cells, SOD inhibition in HUVECs/si-NC and HUVECs/siCav-1 was significantly decreased by LPS (75 µg/ml). In addition, ACh stimulation caused a greater increase in [Ca2+]i in HUVECs/si-NC as compared with LPS-treated HUVECs/si-NC. ACh stimulation also induced significantly higher NO levels in LPS-treated HUVECs/siCav-1 compared with LPS-treated HUVECs/si-NC cells (P<0.05). In conclusion, the downregulated Cav-1 expression served a key role in NO production in the in vitro model of CAS induced by ACh stimulation of LPS-damaged HUVECs.

Persisting Angina after Successful Surgical Removal of a Large Coronary Artery Aneurysm Attached to the Proximal Portion of the Left Circumflex Artery: Role of Coronary Artery Spasm

Persisting Angina after Successful Surgical Removal of a Large Coronary Artery Aneurysm Attached to the Proximal Portion of the Left Circumflex Artery: Role of Coronary Artery Spasm

Impact of endothelial dysfunction by FMD on long-term outcomes of coronary artery spasm induced by acetylcholine provocation test-EAS 2017

Aim: Endothelial dysfunction (ED) plays a major role in coronary artery spasm (CAS). However, there is no study that investigated the impact of ED on prognosis in patients with CAS induced by the acetylcholine provocation test (ACH-test).

Enhanced transient receptor potential channel-mediated Ca2+ influx in the cells with phospholipase C-δ1 overexpression: its possible role in coronary artery spasm.

We reported that coronary spasm was induced in the transgenic mice with the increased phospholipase C (PLC)-δ1 activity. We investigated the effect of enhanced PLC-δ1 on Ca2+ influx and its underlying mechanisms. We used human embryonic kidney (HEK)-293 and coronary arteries smooth muscle cells (CASMC). Intracellular free Ca2+ concentration ([Ca2+ ]i ; nm) was measured by fura-2, and Ca2+ influx was evaluated by the increase in [Ca2+ ]i after addition of extracellular Ca2+ . Acetylcholine (ACh) was used to induce Ca2+ influx. ACh-induced peak Ca2+ influx was 19 ± 3 in control HEK-293 cells and 71 ± 8 in the cells with PLC-δ1 overexpression (P < 0.05 between two groups). Nifedipine partially suppressed this Ca2+ influx, whereas either 2-APB or knockdown of classical transient receptor potential channel 6 (TRPC6) blocked this Ca2+ influx. In the human CASMC, ACh-induced peak Ca2+ influx was 29 ± 6 in the control and was increased to 45 ± 16 by PLC-δ1 overexpression (P < 0.05). Like HEK-293 cells, pretreatment with nifedipine partially suppressed Ca2+ influx, whereas either 2-APB or knockdown of TRPC6 blocked it. ACh-induced Ca2+ influx was enhanced by PLC-δ1 overexpression, and was blocked partially by nifedipine and completely by 2-APB. TRPC-mediated Ca2+ influx may be related to the enhanced Ca2+ influx in PLC-δ1 overexpression.

Age-related oxidant stress with senescence marker protein-30 deficiency plays a pivotal role in coronary artery spasm

We examined the mechanism of coronary artery spasm related to oxidant stress with aging in senescence marker protein-30 (SMP30)-deficient mice because SMP30 decreases with aging and SMP30 knockout (KO) mice show a short life with increased oxidant stress. To examine the effect of SMP30 on coronary artery vasomotor tone, we measured the endothelium-dependent [5-hydroxytryptamine (5-HT)] response of isolated, pressurized coronary arteries from SMP30 KO and wild-type (WT) mice (n=10 each). In SMP30 KO mice, 5-HT-induced vasoconstriction occurred, which altered vasodilation with dithiothreitol, a thiol-reducing agent. In WT mice, 5-HT-induced vasodilation occurred. Administration of 5-HT from the aortic sinus induced a coronary artery spasm in SMP30 KO mice, which was prevented by the intravenous administration of Y-27632, rho-kinase inhibitor. The fluorescence level of monochlorobimane in coronary arteries, which covalently labels the reduced total thiols, decreased in SMP30 KO mice, but reverted to a level comparable with that of WT mice on treatment with Y-27632. From these results, SMP30 provides protection against coronary artery spasm. Chronic oxidant stress associated with aging plays an important role in coronary artery spasm related to thiol oxidation and rho-kinase signaling.

Ventricular Tachycardia Complicating Head‐up Tilt Test: The role of Coronary Artery Spasm

Head-up tilt test (HUT) is frequently used for diagnosis of neurocardiogenic syncope. It mimics orthostatic stress resulting in venous pooling, central hypovolemia with compensated left ventricular hypercontraction, and sympathetic stimulation. Although generally considered to be a safe procedure, we hereby present a rare complication of HUT in a 50-year-old woman with isoproterenol infusion inducing coronary spasm that resulted in ventricular tachycardia.

Rapid Progression of Coronary Atherosclerosis by Coronary Artery Spasm Leading to Acute Coronary Syndrome

HomeCirculationVol. 119, No. 16Rapid Progression of Coronary Atherosclerosis by Coronary Artery Spasm Leading to Acute Coronary Syndrome Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBRapid Progression of Coronary Atherosclerosis by Coronary Artery Spasm Leading to Acute Coronary Syndrome Ichiro Sakamoto, Masahiro Mohri and Hideo Yamamoto Ichiro SakamotoIchiro Sakamoto From the Department of Cardiology, Kyushu Kosei-Nenkin Hospital, Kitakyushu, Japan. Search for more papers by this author , Masahiro MohriMasahiro Mohri From the Department of Cardiology, Kyushu Kosei-Nenkin Hospital, Kitakyushu, Japan. Search for more papers by this author and Hideo YamamotoHideo Yamamoto From the Department of Cardiology, Kyushu Kosei-Nenkin Hospital, Kitakyushu, Japan. Search for more papers by this author Originally published28 Apr 2009https://doi.org/10.1161/CIRCULATIONAHA.108.839522Circulation. 2009;119:2233–2234A 67-year-old normotensive, normolipidemic man presented with short-lasting chest pain followed by syncope. Intracoronary ergonovine maleate (40 μg) provoked a severe spasm in the middle portion of right coronary artery (Figure 1A and 1B, arrow), but there was no significant (>50%) right or left coronary artery disease after intracoronary nitrates (Figure 1C). The patient was diagnosed as having vasospastic angina. Download figureDownload PowerPointFigure 1. Right coronary arteriograms before (A) and after intracoronary ergonovine (B) and isosorbide dinitrate (ISDN; C).Three years later, he presented with sustained, nitroglycerin-resistant chest pain at our emergency room. Emergent coronary arteriography revealed a high-grade stenosis where coronary spasm had been documented earlier (Figure 2A, arrow). Intracoronary administration of isosorbide dinitrate improved distal filling but failed to dilate the stenosed segment (Figure 2B). Intravascular ultrasound confirmed coronary plaque at that segment (Figure 2B, inset), and a bare metal stent was successfully implanted (Figure 2C). Serial changes in serum enzymes confirmed the diagnosis of acute non–ST-elevation myocardial infarction. Download figureDownload PowerPointFigure 2. Right coronary arteriograms before (A) and after intracoronary isosorbide dinitrate (ISDN; B) and percutaneous coronary intervention (PCI; C).Although coronary spasm has been implicated to cause atherosclerosis progression over years,1 there are few reports demonstrating a critical role of coronary artery spasm in rapid plaque progression and the development of acute coronary syndrome. Because there was no disease progression in left coronary artery segments, it was assumed that focal spasm might have contributed to a ruptured atheromatous plaque in our patient, leading eventually to myocardial infarction. Previous experimental studies have shown that coronary artery spasm could cause intraplaque hemorrhage and acute myocardial infarction in the swine model.2 Thus, coronary vasospasm may play an important role in the pathogenesis of not only variant angina but also acute coronary syndrome, as seen in this patient.DisclosuresNone.FootnotesCorrespondence to Masahiro Mohri, MD, PhD, Department of Cardiology, Kyushu Kosei-Nenkin Hospital, 1-8-1 Kishinoura, Kitakyushu 806-8501, Japan. E-mail [email protected]References1 Nobuyoshi M, Tanaka M, Nosaka H, Kimura T, Yokoi H, Hamasaki N, Kim K, Shindo T, Kimura K. Progression of coronary atherosclerosis: is coronary spasm related to progression? J Am Coll Cardiol. 1991; 18: 904–910.CrossrefMedlineGoogle Scholar2 Kuga T, Tagawa H, Tomoike H, Mitsuoka W, Egashira S, Ohara Y, Takeshita A, Nakamura M. Role of coronary artery spasm in progression of organic coronary stenosis and acute myocardial infarction in a swine model: importance of mode of onset and duration of coronary artery spasm. Circulation. 1993; 87: 573–582.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kim J, Park J, Yang Y, Lee S, Kim D, Song J, Kang D, Park S, Park S and Song J (2022) Percutaneous coronary intervention in patients with documented coronary vasospasm during long-term follow-up, Heart, 10.1136/heartjnl-2021-320645, 108:16, (1303-1309), Online publication date: 1-Aug-2022. Mori H, Takahashi J, Sato K, Miyata S, Takagi Y, Tsunoda R, Sumiyoshi T, Matsui M, Tanabe Y, Sueda S, Momomura S, Kaikita K, Yasuda S, Ogawa H, Shimokawa H and Suzuki H (2020) The impact of antiplatelet therapy on patients with vasospastic angina: A multicenter registry study of the Japanese Coronary Spasm Association, IJC Heart & Vasculature, 10.1016/j.ijcha.2020.100561, 29, (100561), Online publication date: 1-Aug-2020. Montenegro Sá F, Ruivo C, Graça Santos L, Antunes A, Soares F, Baptista J and Morais J (2018) Ultra-rapid progression of coronary artery disease or undiagnosed unstable plaque? A brief review from a case report, Revista Portuguesa de Cardiologia (English Edition), 10.1016/j.repce.2018.02.016, 37:3, (259-264), Online publication date: 1-Mar-2018. Montenegro Sá F, Ruivo C, Graça Santos L, Antunes A, Campos Soares F, Baptista J and Morais J (2018) Progressão ultrarrápida de doença coronária ou placa instável não detetada?, Revista Portuguesa de Cardiologia, 10.1016/j.repc.2017.04.005, 37:3, (259-264), Online publication date: 1-Mar-2018. Shah P, Bajaj S, Virk H, Bikkina M and Shamoon F (2015) Rapid Progression of Coronary Atherosclerosis: A Review, Thrombosis, 10.1155/2015/634983, 2015, (1-6), Online publication date: 28-Dec-2016. April 28, 2009Vol 119, Issue 16 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.108.839522PMID: 19398679 Originally publishedApril 28, 2009 PDF download Advertisement SubjectsAcute Coronary Syndromes

Preference toward a T-helper type 1 response in patients with coronary spastic angina.

Coronary artery spasm plays an important role in the pathogenesis of ischemic heart diseases such as unstable angina (UA) and acute myocardial infarction. Nitric oxide (NO) plays an important role in coronary artery spasm. We previously reported a deficiency in NO activity in the spasm arteries of patients with coronary spastic angina (CSA). Others have reported that NO influences the immune response. Therefore, we investigated the balance between T-helper type 1 (Th1) and 2 (Th2) responses in patients with CSA by evaluating the frequencies of interferon (IFN)-gamma-producing T cells and interleukin (IL)-4-producing T cells in the peripheral blood of such patients. Peripheral blood mononuclear cells were collected from 50 consecutive patients with CSA, 23 consecutive patients with UA, 36 patients with stable angina (SA), and 21 patients with chest pain syndrome (CPS). Cytokine-producing CD4+ T cells were quantified by 3-color flow cytometry after stimulation with phorbol myristate acetate and ionomycin. UA and CSA were associated with a significant increase in the frequency of CD4+ T cells that produced IFN-gamma, whereas these conditions caused no significant difference in the frequency of CD4+ T cells that produced IL-4. Culturing with an NO donor compound for 24 hours before stimulation inhibited the increase in the frequency of CD4+ T cells that produced IFN-gamma. We demonstrated that there was a preference toward the Th1-type response in patients with CSA and that T cells showed a reduced Th1-type response after being treated with NO.

Sphingosine 1-phosphate induces contraction of coronary artery smooth muscle cells via S1P2.

Sphingosine 1-phosphate (Sph-1-P), a bioactive lipid derived from activated platelets, may play an important role in coronary artery spasm and hence the pathogenesis of ischemic heart diseases, since we reported that a decrease in coronary blood flow was induced by this lysophospholipid in an in vivo canine heart model [Cardiovasc. Res. 46 (2000) 119]. In this study, metabolism related to and cellular responses elicited by Sph-1-P were examined in human coronary artery smooth muscle cells (CASMCs). [3H]Sphingosine (Sph), incorporated into CASMCs, was converted to [3H]Sph-1-P intracellularly, but its stimulation-dependent formation and extracellular release were not observed. Furthermore, the cell surface Sph-1-P receptors of S1P family (previously called EDG) were found to be expressed in CASMCs. Accordingly, Sph-1-P seems to act as an extracellular mediator in CASMCs. Consistent with Sph-1-P-elicited coronary vasoconstriction in vivo, Sph-1-P strongly induced CASMC contraction, which was inhibited by JTE-013, a newly-developed specific antagonist of S1P(2) (EDG-5). Furthermore, C3 exoenzyme or Y-27632 inhibited the CASMC contraction induced by Sph-1-P, indicating Rho involvement. Finally, exogenously-added [3H]Sph-1-P underwent a rapid degradation. Since lipid phosphate phosphatases, ectoenzymes capable of dephosphorylating Sph-1-P, were expressed in CASMCs, Sph-1-P may be dephosphorylated by the ectophosphatases. Sph-1-P, derived from platelets and dephosphorylated on the cell surface, may induce the contraction of coronary artery smooth muscle cells through the S1P(2)/Rho signaling.

Detection of Platelets Activated during Acetylcholine-Induced Coronary Vasospasm

Although platelet activation may play a role in coronary artery spasm, platelets activated following coronary vasospasm have not been clinically detected. We performed flow cytometric analysis of activation-dependent granular proteins, CD62P (P-selectin), CD63, PAC-1 (activated glycoprotein [GP] IIb/IIIa) and thrombospondin on the platelet plasma membrane in patients who exhibited acetylcholine-induced coronary vasospasm and compared findings with those in control patients without vasospasm. We simultaneously investigated the plasma levels of thrombin anti-thrombin III complex (TAT), plasmin alpha2-plasmin inhibitor complex (PIC), and thrombomodulin. In patients with vasospasm, the expression of CD62P, CD63 and PAC-1 on the platelet membrane surface increased in coronary sinus blood samples following coronary vasospasm, although the expression in aortic samples did not change. The TAT level also increased in the coronary sinus after vasospasm. Platelets might be activated by coronary vasospasm within the coronary circulation. The platelet activation process may be modulated by thrombin generation.

Role of coronary artery spasm in progression of organic coronary stenosis and acute myocardial infarction in a swine model. Importance of mode of onset and duration of coronary artery spasm.

Coronary spasm may play an important role in progression of organic coronary stenosis and myocardial infarction, but the mechanisms responsible for these complications are not known. This study aimed to examine whether the mode of onset and the duration of coronary spasm influenced progression of organic coronary stenosis and acute myocardial infarction in a swine model of coronary spasm. Göttingen miniature pigs were subjected to cholesterol feeding, balloon-induced coronary arterial denudation, and x-ray irradiation. Five months later, coronary spasm was induced by intracoronary injection of serotonin. In 10 pigs, coronary spasm was provoked abruptly and maintained for 25 minutes by five repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes (group A, abrupt onset and short duration). In group B, coronary spasm was provoked gradually by intracoronary injections of serotonin at graded doses of 0.1, 0.3, and 0.6 microgram/kg every 5 minutes and was then maintained for 25 minutes in four pigs (group B1, gradual onset and short duration) and for 120 minutes in six pigs (group B2, gradual onset and long duration) by repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes. Intramural hemorrhage was noted histologically at the spastic site more frequently in group A with abrupt onset (nine of 10 pigs) than in group B with gradual onset (two of 10 pigs) (p < 0.01). Progression of organic coronary stenosis due to intramural hemorrhage was noted in seven pigs (six pigs in group A and one pig in group B), including three cases of total coronary occlusion. Evidence for the evolution of acute myocardial infarction (serial ECG findings, left ventriculograms, and histological findings) was noted in one pig (7%) of group A or B1 with short duration and in five of six pigs (83%) in group B2 with long duration (p < 0.01 versus group A and B1). These results indicate that: 1) intramural hemorrhage was frequently induced by coronary spasm of abrupt but not of gradual onset, 2) intramural hemorrhage resulted in acute progression of coronary stenosis and sometimes resulted in persistent total coronary occlusion leading to acute myocardial infarction, and 3) prolonged coronary spasm resulted in acute myocardial infarction without progression of organic coronary stenosis.

The sensitivity of intracoronary injection of acetylcholine in inducing coronary spasm differs in patients with stable and unstable angina

In an attempt to clarify the role of coronary artery spasm in the pathogenesis of unstable angina, acetylcholine (20 and 50 μg) was injected directly into the coronary arteries of 19 patients with unstable effort angina (group 1), 30 patients with unstable spontaneous angina (group 2), and 15 patients with stable effort angina due to coronary artery organic stenosis (≧ 75%) (group 3). Coronary spasm was defined as severe vasoconstriction (≧ 90% of luminal diameter) with chest pain and/or ischemic ST-segment changes. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 19 patients (100%) of group 1 and 28 (93%) of group 2 but only 3 (20%) of group 3 ( p < 0.01). When acetylcholine was injected into the left and right coronary arteries separately, multivessel spasm (spasm of both coronary arteries) was induced in 5 of 12 (42%) patients of group 1 and in 9 of 23 (39%) patients of group 2. In contrast, intracoronary acetylcholine did not cause multivessel coronary spasm in any of 15 patients of group 3 (0%). These results suggest that coronary arteries in patients with unstable effort angina as well as spontaneous angina are susceptible to spasm and that coronary artery spasm may be responsible at least in part for the genesis of attacks in these patients.

Pathogenesis of unstable angina with 0- or 1-vessel disease. Important role of coronary artery spasm.

In order to examine the possible role of coronary artery spasm in the pathogenesis of unstable angina, provocative testing for coronary spasm was performed in 43 patients with unstable angina who had 0- or 1-vessel disease. Coronary spasm was induced in 20 (65%) of 31 patients by hyperventilation testing (ST increases in 18, ST decreases in 2). Anginal attacks with either ST-segment elevation or ST-segment depression in patients without a significant organic stenosis were induced in 23 (55%) of 42 patients during treadmill exercise testing. Coronary artery spasm, showing severe (> or = 90%) vasoconstriction with angina and/or ischemic electrocardiographic ST-segment deviation, was also documented angiographically in 42 (98%) of 43 patients following intracoronary injection of acetylcholine. We conclude that dynamic coronary obstruction plays an important role in the genesis of attacks in patients with unstable angina who had 0- or 1-vessel organic coronary artery disease.

Importance of coronary artery spasm in alcohol-related unexplained syncope.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

Acute myocardial infarction with normal coronary arteries in a case of polyarteritis nodosa: possible role of coronary artery spasm

A 20 year old man with no previous history of heart disease presented with acute left ventricular failure following extensive anterior wall myocardial infarction. Selective angiography revealed multiple aneurysms in the renal, mesenteric and hepatic arteries with an infarct in the lower pole of the right kidney. These findings, along with the presence of circulating hepatitis B surface antigen favoured the diagnosis of polyarteritis nodosa. In view of normal coronary angiogram and absence of myocardial vasculitis, coronary vasospasm was implicated as the cause of myocardial infarction. Such an occurrence, which could have different therapeutic and diagnostic implications, has not, to our knowledge, been previously described in polyarteritis nodosa.

Quantitative coronary angiography to measure progression and regression of coronary atherosclerosis. Value, limitations, and implications for clinical trials.

HomeCirculationVol. 84, No. 1Quantitative coronary angiography to measure progression and regression of coronary atherosclerosis. Value, limitations, and implications for clinical trials. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBQuantitative coronary angiography to measure progression and regression of coronary atherosclerosis. Value, limitations, and implications for clinical trials. P J de Feyter, P W Serruys, M J Davies, P Richardson, J Lubsen and M F Oliver P J de FeyterP J de Feyter Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author , P W SerruysP W Serruys Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author , M J DaviesM J Davies Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author , P RichardsonP Richardson Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author , J LubsenJ Lubsen Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author and M F OliverM F Oliver Thorax Center, University Hospital, Rotterdam, The Netherlands. Search for more papers by this author Originally published1 Jul 1991https://doi.org/10.1161/01.CIR.84.1.412Circulation. 1991;84:412–423 Previous Back to top Next FiguresReferencesRelatedDetailsCited BySeveri S, Picano E, Michelassi C, Lattanzi F, Landi P, Distante A and L'Abbate A (1994) Diagnostic and prognostic value of dipyridamole echocardiography in patients with suspected coronary artery disease. Comparison with exercise electrocardiography., Circulation, 89:3, (1160-1173), Online publication date: 1-Mar-1994.Agatston A and Janowitz W (1994) Ultrafast computed tomography in coronary screening., Circulation, 89:4, (1908-1909), Online publication date: 1-Apr-1994.Faxon D, Spiro T, Minor S, Coté G, Douglas J, Gottlieb R, Califf R, Dorosti K, Topol E and Gordon J (1994) Low molecular weight heparin in prevention of restenosis after angioplasty. Results of Enoxaparin Restenosis (ERA) Trial., Circulation, 90:2, (908-914), Online publication date: 1-Aug-1994.Kaplan J, Manuck S, Adams M, Williams J, Register T and Clarkson T (1993) Plaque changes and arterial enlargement in atherosclerotic monkeys after manipulation of diet and social environment., Arteriosclerosis and Thrombosis: A Journal of Vascular Biology, 13:2, (254-263), Online publication date: 1-Feb-1993.Kuga T, Tagawa H, Tomoike H, Mitsuoka W, Egashira S, Ohara Y, Takeshita A and Nakamura M (1993) Role of coronary artery spasm in progression of organic coronary stenosis and acute myocardial infarction in a swine model. Importance of mode of onset and duration of coronary artery spasm., Circulation, 87:2, (573-582), Online publication date: 1-Feb-1993. July 1, 1991Vol 84, Issue 1Article InformationMetrics Copyright © 1991 by American Heart Associationhttps://doi.org/10.1161/01.CIR.84.1.412 Originally publishedJuly 1, 1991 PDF download Advertisement

Circadian Influence in Cardiovascular Disease (Part 1)

This department will offer stylized clinical presentations of current cardiovascular issues. Questions raised as a case history evolves highlight key elements that are elaborated upon in the discussions which follow.

Possible role of coronary artery spasm in unexplained syncope

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 ± 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of ≥75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. In 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiotogic study. These results suggest that coronary spasm is involved in unexplained syncope.