Relation Between Cancer and Vasospastic Angina.
Ontology highlight
ABSTRACT: Introduction
Patients with cancer have an increased risk of cardiovascular disease including ischemic heart disease and vice versa. Anticancer drugs and radiotherapy are known to contribute to endothelial injury and vasospasm. However, the relations between vasospastic angina (VSA) and cancer or its treatment are poorly investigated.Methods
A total of 786 patients underwent intracoronary acetylcholine (ACh) provocation tests to diagnose VSA. The positive ACh provocation test was defined as angiographic coronary artery spasm accompanied by chest pain and/or ischemic electrocardiographic changes. Patients were divided into active cancer, a history of cancer, and no cancer according to the status of malignancy. The impact of types of cancer, anticancer drugs, and radiotherapy on VSA was evaluated.Results
Of 786 patients, 38 (4.8%) and 84 (10.7%) had active cancer and a history of cancer, respectively, and 401 (51.0%) were diagnosed as VSA. There was no significant difference in rates of positive ACh test among patients with active cancer, a history of cancer, and no cancer (39.5% vs. 57.1% vs. 50.9%, p = 0.20). Types of cancer and cancer treatment also had no impact on positive ACh provocation test.Conclusions
In this cross-sectional observational study, we did not find an association of active and a history of cancer with the diagnosis of VSA. Anticancer treatment including chemotherapy and radiotherapy was not significantly associated with positive ACh provocation test.
SUBMITTER: Matsumoto T
PROVIDER: S-EPMC8342335 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:AimsCoronary microvascular dysfunction and/or vasospasm are potential causes of ischaemia in patients with no obstructive coronary artery disease (INOCA). We tested the hypothesis that these patients also have functional abnormalities in peripheral small arteries.Methods and resultsPatients were prospectively enrolled and categorised as having microvascular angina (MVA), vasospastic angina (VSA) or normal control based on invasive coronary artery function tests incorporating probes of endothelial and endothelial-independent function (acetylcholine and adenosine). Gluteal biopsies of subcutaneous fat were performed in 81 subjects (62 years, 69% female, 59 MVA, 11 VSA, and 11 controls). Resistance arteries were dissected enabling study using wire myography. Maximum relaxation to ACh (endothelial function) was reduced in MVA vs. controls [median 77.6 vs. 98.7%; 95% confidence interval (CI) of difference 2.3-38%; P = 0.0047]. Endothelium-independent relaxation [sodium nitroprusside (SNP)] was similar between all groups. The maximum contractile response to endothelin-1 (ET-1) was greater in MVA (median 121%) vs. controls (100%; 95% CI of median difference 4.7-45%, P = 0.015). Response to the thromboxane agonist, U46619, was also greater in MVA (143%) vs. controls (109%; 95% CI of difference 13-57%, P = 0.003). Patients with VSA had similar abnormal patterns of peripheral vascular reactivity including reduced maximum relaxation to ACh (median 79.0% vs. 98.7%; P = 0.03) and increased response to constrictor agonists including ET-1 (median 125% vs. 100%; P = 0.02). In all groups, resistance arteries were ≈50-fold more sensitive to the constrictor effects of ET-1 compared with U46619.ConclusionsSystemic microvascular abnormalities are common in patients with MVA and VSA. These mechanisms may involve ET-1 and were characterized by endothelial dysfunction and enhanced vasoconstriction.Clinical trial registrationClinicalTrials.gov registration is NCT03193294.
| S-EPMC6284165 | biostudies-literature
Project description:We herein report a case of a 56-year-old woman with angina pectoris. She visited our emergency room because of chest pain. She finally underwent emergency percutaneous coronary intervention in right coronary artery due to acute coronary syndrome. Several months later, she complained of exertional chest pain again. Exercise-stress electrocardiogram showed ST-segment depression in V2-V6. However, coronary angiography showed no organic stenosis and we conducted acetylcholine provocation test. We finally detected severe coronary artery spasm and diagnosed exercise-induced vasospastic angina (VSA). This case highlights the importance of the recognition of exercise-induced VSA. Exercise-induced VSA needs the definite diagnosis and appropriate treatment. Learning objective Many patients felt chest pain even if they have undergone percutaneous coronary intervention (PCI). This case highlights the importance of the recognition of exercise-induced vasospastic angina (VSA). Exercise-induced VSA needs definite diagnosis and appropriate treatment. This case report describes the importance of precise diagnosis and highlights the recognition of exercise-induced VSA. We recommend the acetylcholine provocation test after PCI in order to determine the diagnosis of exercise-induced VSA.
| S-EPMC8758595 | biostudies-literature
Project description:BackgroundSympathetic overactivity has been linked to vasospastic angina (VSA), although the exact pathophysiology of VSA is poorly understood. The purpose of this study is to assess if renal sympathetic denervation (RDN) reduces cardiac sympathetic nerve activity with a subsequent beneficial effect on angina relief in patients with refractory VSA.Methods and resultsCardiac sympathetic nerve activity was assessed prior to procedure and at 6 months post-procedure using iodine-123 labeled meta-iodobenzylguanidine (123I-MIBG) imaging. The Seattle Angina questionnaire (SAQ) was used to assess the degree to which the disease impacts quality of life. No significant change was observed in early HMR (pre-RDN: 2.74 [2.10 to 3.21] vs 6 months post-RDN: 2.57 [2.20 to 3.00]; P = 0.76), and late HMR (pre-RDN: 2.56 [2.18 to 3.20] vs 6 months post-RDN: 2.36 [2.13 to 3.22]; P = 0.22). Additionally, no change was seen in WR (P = 0.22). SAQ results revealed significant improvements in perceived physical limitation, angina frequency, and quality of life at 6 months (P < 0.05 for all).ConclusionRDN resulted in improvements in angina class and quality of life at 6 months in patients with refractory VSA. RDN, however, did not result in significant changes in cardiac sympathetic nerve activity as measured using 123I-MIBG. The latter observation should be considered with caution given the small sample size of this study. Larger studies are needed to assess this further.
| S-EPMC7749092 | biostudies-literature
Project description:Hypokalemia is a common electrolyte disturbance and is related to poor prognosis in patients with cardiovascular disease. However, the role of hypokalemia in patients with vasospastic angina (VSA) has not yet been studied. The present study enrolled 1454 patients diagnosed with VSA according to ergonovine provocation test results and available admission serum potassium data. The primary outcome was a composite of cardiac death, acute coronary syndrome, and new-onset life-threatening arrhythmia. Based on a hypokalemia definition as serum potassium concentration ≤ 3.5 mEq/L, the hypokalaemia group included 70 patients (4.8%). The median potassium levels were 3.4 mEq/L [interquartile range (IQR) 3.3-3.5] in the hypokalemia group and 4.1 mEq/L (IQR 3.9-4.3) in the no-hypokalemia group. The median follow-up duration was 764 days. Primary outcomes occurred in seven patients (10.0%) in the hypokalemia group and 51 patients (3.7%) in the no-hypokalemia group. The Kaplan-Meier analysis showed a higher cumulative incidence of primary outcomes in the hypokalemia group compared to that in the no-hypokalemia group (log-rank P = 0.014). Multivariate Cox regression analysis also showed that hypokalemia was an independent predictor of primary outcomes. In conclusion, hypokalemia at admission was associated with adverse clinical outcomes in VSA.
| S-EPMC7952915 | biostudies-literature
Project description:BACKGROUND AND OBJECTIVES:Recent studies indicate that in response to vasoconstrictor stimuli, the small GTPase RhoA and its down-stream effector, Rho-associated kinase 2 (ROCK)/Rho-kinase, are associated with hypercontraction of the vascular smooth muscle of coronary arteries through augmentation of myosin light chain phosphorylation and Ca(2+) sensitization. Expression of ROCK/Rho-kinase mRNA was significantly increased and up-regulated in the spastic coronary artery in a porcine model, and a specific inhibitor of ROCK/Rho-kinase inhibited coronary artery spasm in humans. We therefore explored the role of ROCK2 polymorphisms in the pathogenesis of vasospastic angina (VA). SUBJECTS AND METHODS:We studied 106 patients with VA who exhibited spontaneous or provoked coronary spasm during coronary angiography and compared the prevalence of ROCK2 polymorphisms between this group of patients with VA and controls whose angiograms were normal, and in whom the ergonovine test did not cause spasm (n=107). Five single nucleotide polymorphisms (SNPs) of the ROCK2 gene were selected. SNPs were genotyped by high-resolution melting. Linkage disequilibrium and haplotype analyses were performed using the SHEsis program. RESULTS:The prevalence of genotypes of the 5 interesting SNPs in patients with VA was not different from that in the control group. In haplotype analysis, the haplotype G-T-C-T-G (in order of rs978906, rs2271621, rs2230774, rs1515210, and rs3771106) was significantly associated with a decreased risk of VA (p=0.007). CONCLUSION:The haplotype G-T-C-T-G in the ROCK2 gene had a protective effect against VA, suggesting the involvement of ROCK2 in VA pathogenesis.
| S-EPMC3390426 | biostudies-literature
Project description:Vasospastic angina (VSA) is characterized by a reversible spasm of the coronary arteries and is more prevalent in Asians. Vasodilators, such as calcium channel blockers, are effective in relieving coronary spasms and preventing clinical events. Therefore, the prognosis of VSA is generally known to be better than for significant organic stenosis caused by atherosclerosis. However, coronary vasospasm is sometimes associated with fatal complications such as sudden death, ventricular arrhythmia, and myocardial infarction. Thus, it is very important to identify and actively treat high-risk patients to prevent VSA complications. Here, we will review clinical factors associated with long-term prognosis in patients with VSA.
| S-EPMC8469875 | biostudies-literature
Project description:There is an accumulating body of evidence indicating association between inflammation and the pathogenesis of coronary vasospastic angina (CVA). Interleukin-6 (IL-6) is a pleiotropic cytokine, functions as a mediator of inflammatory response and has both pro-inflammatory and anti-inflammatory properties. The aim of the present study is to investigate the association of -634C/G polymorphism of IL-6 gene with CVA in Han Chinese. A total of 27 CVA patients and 232 healthy controls were eligible for this study. The PCR-based restriction fragment length polymorphism (PCR-RFLP) technique was used to assess the genotypes frequencies. The distribution of the IL-6 -634C/G genotypes (CC, CG, and GG) was 59.48%, 37.07%, and 3.45% in the controls, and 37.04%, 48.15%, and 14.81% in CVA group, respectively (P = 0.0080). The frequency of the G allele in the CVA group was significantly higher than that in the control group (38.89% vs 21.98%, P = 0.0057). Compared with the wild type CC, the G allele carriers (CG + GG genotypes) had increased risk of CVA in both unadjusted and adjusted analyses. These findings suggest that IL-6 -634C/G polymorphism is associated with CVA and the G allele is an independent risk for CVA in Han Chinese.
| S-EPMC4211799 | biostudies-literature
Project description:Although an angina attack by vasospastic angina (VSA) can usually be relieved or controlled with nitrates and calcium channel blockers (CCBs), there are some patients who cannot be controlled even by higher doses and combinations of these drugs. Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular cyclic adenosine monophosphate (cAMP) contents. A stimulation of cAMP signal transduction increases coronary nitric oxide production. We examined whether cilostazol improved angina symptoms in patients with VSA uncontrolled by conventional treatment.This study was conducted in a prospective, multicenter, nonrandomized manner. The subject consisted of 21 patients (13 men, 57 ± 9 year-old) who were diagnosed with VSA and had at least two angina attacks during the past 1 week despite of conventional medications such as CCBs and/or nitrates. They took cilostazol 100 mg twice daily for 2 weeks in addition to the conventional medications. The patients recorded the frequency of angina attack and wrote down the numeric rating scale of a "severity of angina attack" while taking conventional medications and cilostazol for 2 weeks, and also recorded an averaged scale or total number of event during the last week at the time of the assessment. Using the Wilcoxon rank-sum test, we compared the changes in the scores of frequency and severity of angina attack before and after adding cilostazol to the conventional medications.After adding cilostazol to the conventional medications, there were 78.9% relative reduction of the score of angina intensity and 73.5% of angina frequency (P < 0.001). There were four patients (19%) who were forced to stop cilostazol due to headache as an adverse event.Cilostazol appears to be an effective therapy in VSA uncontrolled with conventional medical treatment. A further prospective, randomized, placebo-controlled study will be needed to validate this result.
| S-EPMC3654168 | biostudies-literature
Project description:We investigated the diagnostic value and pathophysiological role of circulating microRNA (miR) in vasospastic angina (VA). We enrolled patients who underwent coronary angiography for chest pain to explore the miR's diagnostic utility. In addition, we investigated the role of miRs in regulating endothelial nitric oxide synthase (eNOS) expression in human coronary artery endothelial cells (hCAECs). Among the 121 patients, 46 were diagnosed with VA (VA group), 26 with insignificant coronary lesions (ICL group), and 49 with atherothrombotic angina (AA group). The VA group showed a significantly higher expression of miR-17-5p, miR-92a-3p, and miR-126-3p than the ICL group. In contrast, miR-221-3p and miR-222-3p were upregulated in the AA group compared to the VA group, and all levels of miR-17-5p, miR-92a-3p, miR-126-3p, miR-145-5p, miR-221-3p, and miR-222-3p differed between the AA group and the ICL group. In the hCAECs, transfection with mimics (pre-miR) of miR-17-5p, miR-92a-3p, and miR-126-3p was associated with eNOS suppression. Additionally, transfection with inhibitors (anti-miR) of miR-92a-3p significantly rescued the eNOS suppression induced by lipopolysaccharide. In conclusion, the circulating miRs not only proved to have diagnostic utility, but also contributed to pathogenesis by eNOS regulation.
| S-EPMC7290712 | biostudies-literature
Project description:BackgroundNilotinib, a second-generation BCR-ABL tyrosine kinase inhibitor (TKI), is highly effective in the treatment of patients with chronic myeloid leukemia (CML), despite being more vasculotoxic than older TKIs such as imatinib. Herein, we present a case of nilotinib-associated vasospastic angina confirmed by an acetylcholine spasm provocation test.Case presentationA 62-year-old CML patient treated with 300 mg nilotinib twice daily complained of several episodes of rest angina and was hospitalized at our institution. Coronary angiography revealed no severe organic stenosis, and the acetylcholine spasm provocation test confirmed the diagnosis of vasospastic angina. Although treatment with a calcium channel blocker and nicorandil reduced the frequency of chest pain, angina symptoms continued to occur. At 10 months post discharge, the patient complained of increased frequency of angina; therefore, the nilotinib dosage was reduced to 150 mg twice daily. Consequently, the patient reported a significant improvement in chest symptoms.ConclusionsThis case report highlights the potential vasculotoxic effects of nilotinib. Cardiologists and hematologists should be vigilant for coronary artery spasm as a possible vascular adverse event caused by nilotinib.
| S-EPMC8393793 | biostudies-literature