Intracoronary Nifedipine in Patients Suspected of Perioperative Coronary Spasm

1984 ◽  
pp. 119-125
Author(s):  
R. A. E. Dion ◽  
M. Nijsen-Karelse ◽  
G. Jambroes ◽  
G. Bastianen ◽  
J. F. Hitchcock
Keyword(s):  
Coronary Spasm

Mechanisms of angina in patients with biopsy-proven viral myocarditis: insights from intracoronary acetylcholine testing

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Seitz ◽  
V Martinez Pereyra ◽  
A Hubert ◽  
K Klingel ◽  
R Bekeredjian ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Coronary Spasm ◽  
Viral Myocarditis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Funding Source ◽  
Pathophysiological Mechanism ◽  
Ecg Changes ◽  
Ventricular Ejection Fraction ◽  
Microvascular Spasm

Abstract Background Patients with myocarditis often present with angina pectoris despite unobstructed coronary arteries. The underlying pathophysiological mechanism of angina in these patients remains to be elucidated. Coronary artery spasm is a well-known cause of angina in patients with unobstructed coronary arteries. In this study, we sought to assess the frequency of coronary vasomotor disorders in patients with biopsy-proven viral myocarditis. Methods In total, 700 consecutive patients who underwent endomyocardial biopsy for suspected myocarditis between 2008 and 2018 were retrospectively screened. Of these patients, viral myocarditis was confirmed in 303 patients defined as histological/immunohistological evidence of myocardial inflammation and presence of viral genome confirmed by PCR. Of these patients, 34 patients had angina despite unobstructed coronary arteries and underwent intracoronary acetylcholine (ACh) provocation testing in search of coronary spasm. Epicardial spasm was defined as acetylcholine-induced reproduction of the patient's symptoms associated with ischemic ECG changes and >90% epicardial vasoconstriction. Microvascular spasm was defined as symptom reproduction and ECG changes in the absence of significant epicardial vasoconstriction. Results Patients were 49±16 years old, 62% were male and left ventricular ejection fraction was 54±16%. Most frequent viruses were parvovirus B19 (PVB19, 59%) and human herpes virus 6 (HHV6, 26%), 2 patients had combined PVB19/HHV6 infection and 3 patients other herpesviruses (CMV, EBV, VZV). Epicardial spasm was observed in 10 patients (29%) during ACh testing and microvascular spasm was found in 11 patients (32%). The rate of coronary spasm (epicardial and microvascular) was higher in the PVB19 subgroup compared to HHV6 (80% vs. 33%, p=0.031). In particular, there was a higher prevalence of microvascular spasm in PVB19 compared to HHV6 (45% vs. 0%, p=0.018). Conclusion We observed a high prevalence of microvascular and epicardial spasm in patients with biopsy-proven viral myocarditis suggesting coronary spasm as a potential underlying mechanism for angina in these patients. Microvascular spasm was most often observed in patients with PVB19-associated myocarditis. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Robert-Bosch-Stiftung; Berthold-Leibinger-Stiftung

scholarly journals The interplay between myocardial bridging and coronary spasm in patients with myocardial infarction and non-obstructive coronary arteries: pathogenic and prognostic implications

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
RA Montone ◽  
F Gurgoglione ◽  
MG Del Buono ◽  
MC Meucci ◽  
G Iannaccone ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Unstable Angina ◽  
Coronary Arteries ◽  
Obstructive Coronary Artery Disease ◽  
Coronary Spasm ◽  
Interquartile Range ◽  
Myocardial Bridging ◽  
Adverse Cardiovascular Event ◽  
Provocative Test

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial bridging (MB) is associated with endothelial dysfunction and may represent a cause of angina in patients with non-obstructive coronary artery disease (NOCAD). Purpose  Herein, we assessed the interplay between MB and coronary vasomotor disorders, evaluating also their prognostic relevance in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) or stable NOCAD. Methods We prospectively enrolled consecutive NOCAD patients undergoing intracoronary acetylcholine provocative test to assess the presence of epicardial or microvascular spasm in patients with suspected angina or MINOCA. Myocardial bridging was diagnosed by coronary angiography. The incidence of major adverse cardiac events (MACE), defined as the composite of cardiac death, non-fatal MI and rehospitalisation for unstable angina, was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). Results We enrolled 310 patients (mean age 60.6 ± 11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB was an independent predictor of spasm and MINOCA (p < 0.05). At follow-up (median 22 months, interquartile range [13-32]), patients with MB had a higher rate of MACE and a lower SAQ score (all p < 0.001) compared with patients without MB. The rate of MACE was considerably higher in patients with both spasm and MB than in the remaining patients (12/42 [28.6%] vs. 13/268 [4.8%], p < 0.001). Conclusion Among patients with NOCAD coronary spasm associated with MB predicts a worse clinical presentation with MINOCA and a worse clinical outcome at medium-long term follow-up, thus identifying a high-risk subset of patients with MB with relevant therapeutic implications. MB and clinical outcomesCharacteristicsOverall population(n= 310)Presence of Myocardial bridging(n= 53)Absence of Myocardial bridging(n = 257)p valueMACE [n, (%)]25 (8.1)12 (22.6)13 (5.1)<0.001CV Death [n, (%)]1 (0.3)0 (0.0)1 (0.4)0.649MI occurrence [n, (%)]6 (1.9)2 (3.8)4 (1.6)0.286Hospitalization for unstable angina [n, (%)]18 (5.8)10 (18.9)8 (3.1)< 0.001Recurrent angina [n, (%)]70 (22.6)20 (37.7)50 (19.4)0.004SAQ [median (IQR)]82 [78; 88]78 [68; 84]84 [78; 88]< 0.001Follow-up time [months, median (IQR)]22 [15;32]20 [15; 28]23 [15; 34]0.10CV Cardiovascular; MI: Myocardial Infarction; IQR: InterQuartile Range; MACE: Major Adverse Cardiovascular Event; SAQ: Seattle Angina Questionnaire.Abstract Figure Outcomes

scholarly journals Repurposing Riociguat for Treatment of Refractory Angina Resulting From Coronary Spasm

2021 ◽  
Vol 3 (3) ◽  
pp. 392-396
Author(s):  
Valeria Martínez Pereyra ◽  
Andreas Seitz ◽  
Astrid Hubert ◽  
Sascha Beck ◽  
Ute Hofmann ◽  
...  
Keyword(s):  
Coronary Spasm ◽  
Refractory Angina

Multivessel coronary spasm without electrocardiographic changes

1985 ◽  
Vol 110 (5) ◽  
pp. 1064-1067 ◽  
Author(s):  
Filippo Crea ◽  
George S Abela ◽  
Carl J Pepine
Keyword(s):  
Coronary Spasm ◽  
Electrocardiographic Changes

scholarly journals Eosinophil — Mediated immunological mechanism and inflammation in vasospastic angina — Novel coronary risk factor for coronary spasm —

1996 ◽  
Vol 27 (2) ◽  
pp. 230
Author(s):  
Seiji Umemoto ◽  
Noriko Minamisono ◽  
Takahiro Iwami ◽  
Takahito Yonezawa ◽  
Akihisa Fujii ◽  
...  
Keyword(s):  
Risk Factor ◽  
Coronary Spasm ◽  
Coronary Risk Factor ◽  
Vasospastic Angina ◽  
Coronary Risk ◽  
Immunological Mechanism

Drug infusion through a branch of the aortocoronary vein graft for refractory coronary spasm

1994 ◽  
Vol 58 (3) ◽  
pp. 869-871 ◽  
Author(s):  
Hisanori Mayumi ◽  
Yoshito Kawachi ◽  
Hiroyuki Kohno ◽  
Yuji Akaiwa ◽  
Manabu Hisahara ◽  
...  
Keyword(s):  
Vein Graft ◽  
Coronary Spasm ◽  
Drug Infusion

Repeated sudden cardiac death in coronary spasm: Is IVUS helpful to decide treatment strategy?

2012 ◽  
Vol 154 (3) ◽  
pp. e57-e59 ◽  
Author(s):  
Yae Min Park ◽  
Woong Chol Kang ◽  
Kwen-Chul Shin ◽  
Seung Hwan Han ◽  
Taehoon Ahn ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Treatment Strategy ◽  
Cardiac Death ◽  
Coronary Spasm

Abstract 1918 P122 Protein, a Positive Regulator for Phospholipase C-σ1, Is Upregulated and Involved in Enhanced Calcium Signaling in Human Coronary Spasm

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Reiichi Murakami ◽  
Tomohiro Osanai ◽  
Hirofumi Tomita ◽  
Ken Okumura
Keyword(s):  
Protein Expression ◽  
Phospholipase C ◽  
Protein A ◽  
Coronary Spasm ◽  
Amino Acid Replacement ◽  
Hek293 Cells ◽  
Gene Expressions ◽  
Human Embryonic Kidney Cells ◽  
Control Subjects ◽  
Intracellular Ca

We previously showed that the activity of phospholipase C (PLC)-σ1, a key enzyme for Ca 2+ signaling in the coronary artery smooth muscle, was enhanced threefold in patients with coronary spastic angina (CSA) compared with control subjects. Structural mutation of PLC-σ1 (864G-A) variant with the amino acid replacement of arginine 257 by histidine is one mechanism for the enhanced PLC-σ1 activity, but this was observed in only 10% of CSA patients. PLC-σ1 was shown to be positively regulated by p122 protein. We examined the possible role of p122 protein in the mechanism for enhanced PLC-σ1 activity. In 11 patients with CSA and 9 control subjects without CSA, skin fibroblasts were obtained at the coronary angiography and were cultured. Protein and gene expressions of p122 were determined by Western blot analysis and real-time quantitative RT-PCR, respectively. The protein expression of p122 was enhanced in CSA threefold compared with control subjects (237±17 vs 85±13 units, p<0.0001). The gene expression of p122 was also enhanced in CSA by 36.1±8.7% compared with control (p<0.01). We further examined whether the upregulated p122 protein is associated with the enhancement of intracellular Ca 2+ signaling. Human embryonic kidney cells (HEK293) were cultured and transfected by muscarine M1 receptor. In the cells expressing normal PLC-σ1, acethylcholine (ACh) at 10 −6 and 10 −5 mol/L caused a dose-dependent, rapid transient increase in [Ca 2+ ] i followed by a lower but sustained phase of the increase. We further transfected the HEK293 cells by p122, which resulted in the increased expression of p122 protein two-to threefold. [Ca 2+ ] i at baseline was 23±1 nmol/L in the cells without p122 transfection and 39±2 nmol/L in those with p122 (P<0.01). The peak increase in [Ca 2+ ] i from the baseline after ACh was significantly greater in the cells transfected with p122 than in those without transfection (68±6 versus 33±4 nmol/L at 10 −6 mol/L Ach, and 128±11 versus 67±8 nmol/L at 10 −5 mol/L ACh, both P<0.01). The sustained phase of [Ca 2+ ] i increase was prolonged in the cells with p122 transfection compared with those without transfection. In conclusion, the enhanced p122 protein expression is involved in the pathogenesis of CSA by enhancing intracellular Ca 2+ signaling.

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