Myocardial Infarction and Persistent Angina With No Obstructive Coronary Artery Disease.
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ABSTRACT:
SUBMITTER: Malas W
PROVIDER: S-EPMC8301521 | biostudies-literature | 2020 Jan
REPOSITORIES: biostudies-literature
Publications
Myocardial Infarction and Persistent Angina With No Obstructive Coronary Artery Disease.
Malas Waddah W AlBadri Ahmed A Wei Janet J Mehta Puja K PK Anderson R David RD Petersen John J Thomson Louise E LE Pepine Carl J CJ Bairey Merz C Noel CN
JACC. Case reports 20200115 1
Women with myocardial infarction with no obstructive coronary artery disease (MINOCA) are increasingly recognized. Women with MINOCA are at high risk for major adverse cardiovascular events. In this case, we focus on the importance of early identification and management of MINOCA to improve patients' angina and related quality of life. (<b>Level of Difficulty: Beginner.</b>). ...[more]
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Project description:BackgroundMyocardial infarction (MI) patients without obstructive coronary artery disease (CAD) are at increased risk for recurrent ischemic events, but angina frequency post-MI has not been described.Methods and resultsAmong MI patients who underwent angiography, we assessed angina at baseline, 1, 6, and 12 months using the Seattle Angina Questionnaire (SAQ). A hierarchical repeated measures modified Poisson model assessed the association between the absence of obstructive CAD (defined as epicardial stenoses >70% or left main >50%) and angina. Among 5539 MI patients from 31 US hospitals (mean age 60, 68% male), 6.9% had no angiographic obstructive CAD. More patients without obstructive CAD (vs. obstructive CAD) were female (57% vs 30%), non-white (51% vs 24%) and had NSTEMI (87% vs 51%). In unadjusted analyses, patients without obstructive CAD had less angina prior to MI but more angina and worse health status post-discharge. After adjustment for socio-demographic and clinical factors, the risk of post-MI angina was similar in patients without vs. with obstructive CAD (IRR=0.89, 95% CI 0.77-1.02). Among patients without obstructive CAD, depression and self-reported avoidance of care due to cost were independently associated with angina (IRR=1.28 per 5 points on PHQ, 95% CI 1.17-1.41; IRR=1.34, 95% 1.02-1.1.74).ConclusionsFollowing MI, patients without obstructive CAD experience an angina burden at least as high as those with obstructive CAD, affecting 1 in 4 patients at 12 months. As these patients are not candidates for revascularization, other anti-anginal strategies are needed to improve their health status and quality of life.
| S-EPMC5321550 | biostudies-literature
Project description:BackgroundCoronary artery spasm can occur either in response to drugs or toxins. This response may result in hyper-reactivity of vascular smooth muscles or may occur spontaneously as a result of disorders in the coronary vasomotor tone. Hyperthyroidism is associated with coronary artery spasm.Case summaryA 49-year-old female patient with a 2-day history of intermittent chest pain and electrocardiographic evidence of myocardial ischaemia was referred for emergency coronary angiography. This revealed severe right coronary artery (RCA) and left main (LM) coronary artery ostial vasospasm, both subsequently relieved with administration of multiple doses intracoronary nitroglycerine. Intravascular optical coherence tomography showed absence of atherosclerosis and no evidence of thrombus or dissection confirming the diagnosis of coronary artery vasospasm. Laboratory tests of the thyroid function were performed immediately after coronary angiography revealing Graves' disease as the cause of vasospasm.DiscussionOur case represents a rare presentation of Graves' disease-induced RCA and LM coronary artery ostial vasospasm. In patients with coronary artery vasospasm thyroid function study should be mandatory, especially in young female patients.
| S-EPMC7501938 | biostudies-literature
Project description:AimsAngina and no obstructive coronary artery disease (ANOCA) is common. A potential cause of angina in this patient population is a myocardial bridge (MB). We aimed to study the anatomical and haemodynamic characteristics of an MB in patients with ANOCA.Methods and resultsUsing intravascular ultrasound (IVUS), we identified 184 MBs in 154 patients. We evaluated MB length, arterial compression, and halo thickness. MB muscle index (MMI) was defined as MB length×halo thickness. Haemodynamic testing of the MB was performed using an intracoronary pressure/Doppler flow wire at rest and during dobutamine stress. We defined an abnormal diastolic fractional flow reserve (dFFR) as ≤0.76 during stress. The median MB length was 22.9 mm, arterial compression 30.9%, and halo thickness 0.5 mm. The median MMI was 12.1. Endothelial and microvascular dysfunction were present in 85.4% and 22.1%, respectively. At peak dobutamine stress, 94.2% of patients had a dFFR ≤0.76 within and/or distal to the MB. MMI was associated with an abnormal dFFR.ConclusionsIn select patients with ANOCA who have an MB by IVUS, the majority have evidence of a haemodynamically significant dFFR during dobutamine stress, suggesting the MB as being a cause of their angina. A comprehensive invasive assessment of such patients during coronary angiography provides important diagnostic information that can guide management.
| S-EPMC9725037 | biostudies-literature
Project description:Even in absence of obstructive coronary artery disease women with angina pectoris have a poor prognosis possibly due to coronary microvascular disease. Coronary microvascular disease can be assessed by transthoracic Doppler echocardiography measuring coronary flow velocity reserve (CFVR) and by positron emission tomography measuring myocardial blood flow reserve (MBFR). Diffuse myocardial fibrosis can be assessed by cardiovascular magnetic resonance (CMR) T1 mapping. We hypothesized that coronary microvascular disease is associated with diffuse myocardial fibrosis.Women with angina, a clinically indicated coronary angiogram with <50 % stenosis and no diabetes were included. CFVR was measured using dipyridamole (0.84 mg/kg) and MBFR using adenosine (0.84 mg/kg). Focal fibrosis was assessed by 1.5 T CMR late gadolinium enhancement (0.1 mmol/kg) and diffuse myocardial fibrosis by T1 mapping using a modified Look-Locker pulse sequence measuring T1 and extracellular volume fraction (ECV).CFVR and CMR were performed in 64 women, mean (SD) age 62.5 (8.3) years. MBFR was performed in a subgroup of 54 (84 %) of these women. Mean native T1 was 1023 (86) and ECV (%) was 33.7 (3.5); none had focal fibrosis. Median (IQR) CFVR was 2.3 (1.9; 2.7), 23 (36 %) had CFVR < 2 indicating coronary microvascular disease, and median MBFR was 2.7 (2.2; 3.0) and 19 (35 %) had a MBFR value below 2.5. No significant correlations were found between CFVR and ECV or native T1 (R (2) = 0.02; p = 0.27 and R (2) = 0.004; p = 0.61, respectively). There were also no correlations between MBFR and ECV or native T1 (R (2) = 0.1; p = 0.13 and R (2) = 0.004, p = 0.64, respectively). CFVR and MBFR were correlated to hypertension and heart rate.In women with angina and no obstructive coronary artery disease we found no association between measures of coronary microvascular disease and myocardial fibrosis, suggesting that myocardial ischemia induced by coronary microvascular disease does not elicit myocardial fibrosis in this population. The examined parameters seem to provide independent information about myocardial and coronary disease.
| S-EPMC5096323 | biostudies-other
Project description:Atherosclerotic coronary artery disease (CAD) comprises a broad spectrum of clinical entities that include asymptomatic subclinical atherosclerosis and its clinical complications, such as angina pectoris, myocardial infarction (MI) and sudden cardiac death. CAD continues to be the leading cause of death in industrialized society. The long-recognized familial clustering of CAD suggests that genetics plays a central role in its development, with the heritability of CAD and MI estimated at approximately 50% to 60%. Understanding the genetic architecture of CAD and MI has proven to be difficult and costly due to the heterogeneity of clinical CAD and the underlying multi-decade complex pathophysiological processes that involve both genetic and environmental interactions. This review describes the clinical heterogeneity of CAD and MI to clarify the disease spectrum in genetic studies, provides a brief overview of the historical understanding and estimation of the heritability of CAD and MI, recounts major gene discoveries of potential causal mutations in familial CAD and MI, summarizes CAD and MI-associated genetic variants identified using candidate gene approaches and genome-wide association studies (GWAS), and summarizes the current status of the construction and validations of genetic risk scores for lifetime risk prediction and guidance for preventive strategies. Potential protective genetic factors against the development of CAD and MI are also discussed. Finally, GWAS have identified multiple genetic factors associated with an increased risk of in-stent restenosis following stent placement for obstructive CAD. This review will also address genetic factors associated with in-stent restenosis, which may ultimately guide clinical decision-making regarding revascularization strategies for patients with CAD and MI.
| S-EPMC4728103 | biostudies-literature
Project description:AimsThe prognosis of patients with MINOCA (myocardial infarction with non-obstructive coronary arteries) is poorly understood. We examined major adverse cardiac events (MACE) defined as all-cause mortality, re-hospitalization for acute myocardial infarction (AMI), heart failure (HF), or stroke 12-months post-AMI in patients with MINOCA versus AMI patients with obstructive coronary artery disease (MICAD).Methods and resultsMulticentre, observational cohort study of patients with AMI (≥65 years) from the National Cardiovascular Data Registry CathPCI Registry (July 2009-December 2013) who underwent coronary angiography with linkage to the Centers for Medicare and Medicaid (CMS) claims data. Patients were classified as MICAD or MINOCA by the presence or absence of an epicardial vessel with ≥50% stenosis. The primary endpoint was MACE at 12 months, and secondary endpoints included the components of MACE over 12 months. Among 286 780 AMI admissions (276 522 unique patients), 16 849 (5.9%) had MINOCA. The 12-month rates of MACE (18.7% vs. 27.6%), mortality (12.3% vs. 16.7%), and re-hospitalization for AMI (1.3% vs. 6.1%) and HF (5.9% vs. 9.3%) were significantly lower for MINOCA vs. MICAD patients (P < 0.001), but was similar between MINOCA and MICAD patients for re-hospitalization for stroke (1.6% vs. 1.4%, P = 0.128). Following risk-adjustment, MINOCA patients had a 43% lower risk of MACE over 12 months (hazard ratio = 0.57, 95% confidence interval 0.55-0.59), in comparison to MICAD patients. This pattern was similar for adjusted risks of the MACE components.ConclusionThis study confirms an unfavourable prognosis in elderly patients with MINOCA undergoing coronary angiography, with one in five patients with MINOCA suffering a major adverse event over 12 months.
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| S-EPMC11198373 | biostudies-literature
Project description:BackgroundAn association between atherosclerosis and coronary vasospasm has previously been suggested. However, to date, no conclusive data on the whole spectrum of these disorders have been published.AimsThis study aimed to define specific morphological features of atherosclerosis in patients with angina and no obstructive coronary artery disease (ANOCA) due to coronary vasospasm.MethodsFrom February 2019 to January 2020, we enrolled 75 patients referred to our laboratory for a coronary function test (CFT) due to ANOCA and suspected coronary vasomotor dysfunction. The CFT consisted of an acetylcholine test and a physiology assessment with hyperaemic indexes using adenosine. Patients were divided into two groups according to the presence or absence of coronary vasospasm triggered by acetylcholine (ACH+ and ACH-, respectively). In addition, optical coherence tomography (OCT) was performed to assess the lipid index (LI), a surrogate for lipid area, and the prevalence of markers of plaque vulnerability.ResultsACH+ patients had a higher LI than ACH- patients (LI: 819.85 [460.95-2489.03] vs 269.95 [243.50-878.05], respectively, p=0.03), and a higher prevalence of vulnerable plaques (66% vs 38%, p=0.04). Moreover, ACH+ patients showed a higher prevalence of neovascularisation compared to ACH- subjects (37% vs 6%, p=0.02) and a trend towards a higher prevalence of all individual markers, in particular thin-cap fibroatheroma (20% vs 0%, p=0.06). No differences were detected between patterns of coronary vasospasm.ConclusionsThe presence of coronary vasospasm, regardless of its phenotype, is associated with higher lipid burden, plaque vulnerability and neovascularisation.
| S-EPMC10241299 | biostudies-literature
Project description:ImportanceLittle is known about cardiac adverse events among patients with nonobstructive coronary artery disease (CAD).ObjectiveTo compare myocardial infarction (MI) and mortality rates between patients with nonobstructive CAD, obstructive CAD, and no apparent CAD in a national cohort.Design, setting, and participantsRetrospective cohort study of all US veterans undergoing elective coronary angiography for CAD between October 2007 and September 2012 in the Veterans Affairs health care system. Patients with prior CAD events were excluded.ExposuresAngiographic CAD extent, defined by degree (no apparent CAD: no stenosis >20%; nonobstructive CAD: ≥1 stenosis ≥20% but no stenosis ≥70%; obstructive CAD: any stenosis ≥70% or left main [LM] stenosis ≥50%) and distribution (1, 2, or 3 vessel).Main outcomes and measuresThe primary outcome was 1-year hospitalization for nonfatal MI after the index angiography. Secondary outcomes included 1-year all-cause mortality and combined 1-year MI and mortality.ResultsAmong 37,674 patients, 8384 patients (22.3%) had nonobstructive CAD and 20,899 patients (55.4%) had obstructive CAD. Within 1 year, 845 patients died and 385 were rehospitalized for MI. Among patients with no apparent CAD, the 1-year MI rate was 0.11% (n = 8, 95% CI, 0.10%-0.20%) and increased progressively by 1-vessel nonobstructive CAD, 0.24% (n = 10, 95% CI, 0.10%-0.40%); 2-vessel nonobstructive CAD, 0.56% (n = 13, 95% CI, 0.30%-1.00%); 3-vessel nonobstructive CAD, 0.59% (n = 6, 95% CI, 0.30%-1.30%); 1-vessel obstructive CAD, 1.18% (n = 101, 95% CI, 1.00%-1.40%); 2-vessel obstructive CAD, 2.18% (n = 110, 95% CI, 1.80%-2.60%); and 3-vessel or LM obstructive CAD, 2.47% (n = 137, 95% CI, 2.10%-2.90%). After adjustment, 1-year MI rates increased with increasing CAD extent. Relative to patients with no apparent CAD, patients with 1-vessel nonobstructive CAD had a hazard ratio (HR) for 1-year MI of 2.0 (95% CI, 0.8-5.1); 2-vessel nonobstructive HR, 4.6 (95% CI, 2.0-10.5); 3-vessel nonobstructive HR, 4.5 (95% CI, 1.6-12.5); 1-vessel obstructive HR, 9.0 (95% CI, 4.2-19.0); 2-vessel obstructive HR, 16.5 (95% CI, 8.1-33.7); and 3-vessel or LM obstructive HR, 19.5 (95% CI, 9.9-38.2). One-year mortality rates were associated with increasing CAD extent, ranging from 1.38% among patients without apparent CAD to 4.30% with 3-vessel or LM obstructive CAD. After risk adjustment, there was no significant association between 1- or 2-vessel nonobstructive CAD and mortality, but there were significant associations with mortality for 3-vessel nonobstructive CAD (HR, 1.6; 95% CI, 1.1-2.5), 1-vessel obstructive CAD (HR, 1.9; 95% CI, 1.4-2.6), 2-vessel obstructive CAD (HR, 2.8; 95% CI, 2.1-3.7), and 3-vessel or LM obstructive CAD (HR, 3.4; 95% CI, 2.6-4.4). Similar associations were noted with the combined outcome.Conclusions and relevanceIn this cohort of patients undergoing elective coronary angiography, nonobstructive CAD, compared with no apparent CAD, was associated with a significantly greater 1-year risk of MI and all-cause mortality. These findings suggest clinical importance of nonobstructive CAD and warrant further investigation of interventions to improve outcomes among these patients.
| S-EPMC4893304 | biostudies-literature