scholarly journals Pulmonary Arterial Enlargement is Associated With Acute Chest Pain in Patients Without Obstructive Coronary Artery Disease

Author(s):  
Narasa Madam ◽  
Wassim Mosleh ◽  
Natdanai Punnanithinont ◽  
Andres Carmona-Rubio ◽  
Zaid H Said ◽  
...  

Background: Pulmonary hypertension (PH) is an underdiagnosed cause for chest pain in patients without significant coronary artery disease (CAD). Studies showed that enlarged pulmonary arterial (PA) and right ventricular chamber sizes correlate with the severity of PH. Therefore, we studied the association between chest pain, right ventricular dimensions (RVDs), and PA size on coronary coronary tomographic angiography (CCTA). Methods: The CCTA of 87 patients presenting with chest pain without evidence of obstructive CAD was examined. The PA diameter (PAD), right atrial dimension (RAD), and RVD were measured. A comparative control cohort included 31 patients who presented without cardiopulmonary complaints and underwent thoracic CT. The risk for obstructive sleep apnea (OSA) was assessed using STOP-BANG questionnaires. Results: Patients with chest pain without obstructive CAD showed markedly dilated right atrial and ventricular chambers compared with standard parameters (right atrium: 48 ± 6.4 mm; right ventricle long axis: 61 ± 9.5 mm). When comparing chest pain vs non-chest pain group, respectively, the mean PAD measured 25.92 ± 0.43 mm vs 22.89 ± 0.38 mm ( P < .001), RAD2 measured 40.1423 ± 0.7108 mm vs 34.8800 ± 1.0245 mm ( P = .0048), and RVD2 measured 31.7729 ± 0.7299 mm vs 27.6379 ± 1.6178 mm ( P = .034). Chest pain was associated with higher PAD (odds ratio [OR]: 11.11, P < .05) after adjusting for age, sex, body mass index, history of hypertension, hyperlipidemia, congestive heart failure, chronic obstructive pulmonary disease, OSA, and smoking. The chest pain group had a mean STOP-BANG score of 3.9 ± 1.8 in all patients, and 3.62 ± 0.20 in patients without known history of OSA, representing an elevated risk index for the disease. Conclusions: In patients presenting with chest pain without obstructive CAD on CCTA, there is a strong association between the presence of chest pain and enlarged PAD. They also represent a high-risk group for OSA.

2020 ◽  
Vol 9 (1) ◽  
pp. 153-165 ◽  
Author(s):  
Christine Eichelberger ◽  
Aarti Patel ◽  
Zhijie Ding ◽  
Christopher D. Pericone ◽  
Jennifer H. Lin ◽  
...  

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Sheikh Bilal B Khalid ◽  
Javaria Mahmood

Introduction: Cisplatin-based chemotherapeutic regimen (CBCR) is known for increasing risk of venous thromboembolic (TE) disease. We report a unique case of STEMI associated with CBCR which we believe was caused by coronary artery thrombosis. Case description: A 31-yo man with a past history of germ cell tumor presented with chest pain radiating to back and left arm. It started this morning and intensity did not worsen with exertion. He denied any dyspnea, diaphoresis or palpitations. He was non-smoker and non-obese. He denied any family history of premature coronary artery disease. He had undergone unilateral orchiectomy a year ago, and was currently receiving chemotherapy with bleomycin, etoposide and cisplatin; the last dose of his 3 rd cycle was given the day before. EKG showed ST elevation in leads I, aVL, V4 and V5. Troponin I was high to 6.9 ng/ml (ULN 0.045 ng/ml). He received intravenous infusion of thrombolytic. An angiogram done the next day showed moderate mid-LAD disease with residual clot. A CT scan and an echocardiogram later showed left ventricular thrombus (LVT). He was kept on therapeutic enoxaparin along with aspirin. Follow up echocardiogram showed resolution of the thrombus. His chemotherapy was stopped, and he has been kept on active surveillance since then. Discussion: Most cases of CBCR-associated myocardial infarction that have been reported have been seen in the older population with other risk factors for coronary artery disease. Cases where angiographic data was available, coronary artery vasospasm appeared to be the culprit rather than a true plaque rupture. While the presence of LVT raises possibility of thromboembolism to coronaries causing MI, the angiographic findings support accelerated plaque formation to be the cause of infarction. In earlier reports, elevated pre-treatment level of von Willebrand factor has been postulated to have some role in the disease pathogenesis. Other possible mechanisms for pathogenesis include endothelial cell damage, platelet activation, and imbalance between thromboxane-prostacyclin levels. This case emphasizes the need to keep cardiac etiologies of chest pain in the differential when evaluating patients on CBCR as timely intervention is life saving and prevent morbidity.


We describe a case of a 62-year-old man with no previous history of cardiovascular diseases presenting with typical chest pain. The patient was referred for coronary angiography, which revealed the presence of single-vessel coronary artery disease. After intracoronary stent implantation, the patient experienced recurrent episodes of angina followed by further revascularizations that did not clear up his symptoms.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E.-S Im ◽  
I.-S Sohn

Abstract Purposes The aim of this study was to evaluate comparative clinical outcomes of discordant electrocardiographic (ECG) and echocardiographic (Echo) findings compared to concordant findings during treadmill exercise echocardiography in patients with chest pain and no history of coronary artery disease (CAD). Methods A total of 1725 consecutive patients who underwent treadmill echocardiography with chest pain and no history of CAD were screened. The patients were classified into four groups: ECG−/Echo− (negative ECG and Echo), ECG+/Echo− (positive ECG and negative Echo), ECG−/Echo+, and ECG+/Echo+. Concomitant CAD was determined using coronary angiography or coronary computed tomography. Major adverse cardiac events (MACEs) were defined as a composite of coronary revascularization, acute myocardial infarction, and death. Results MACEs were similar between ECG−/Echo− and ECG+/Echo− groups. Compared to ECG+/Echo− group, ECG−/Echo+ group had more MACEs [adjusted hazard ratio (HR) adjusted by clinical risk factors (95% confidence interval), 3.57 (1.75–7.29), p<0.001]. Compared with ECG+/Echo+ group, ECG−/Echo+ group had lower prevalence of concomitant CAD and fewer MACEs [HR, 0.49 (0.29–0.81), p=0.006]. Conclusions Positive exercise Echo alone during treadmill exercise echocardiography had worse clinical outcomes than positive ECG alone, and the latter had similar outcomes to both negative ECG and Echo. Positive exercise Echo alone also had better clinical outcomes than both positive ECG and Echo. Therefore, exercise Echo findings might be superior for predicting clinical outcomes compared to exercise ECG findings. Additional consideration of ECG findings on positive exercise Echo will also facilitate better prediction of clinical outcomes


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