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BACKGROUND: Arterial stiffness is a crucial factor in the pathogenesis of cardiovascular disease, often associated with aging. However, the impact of smoking on arterial stiffness is frequently underestimated. This study aims to investigate the intricate relationship between smoking and arterial stiffness to advance our understanding of and therapeutic approaches to cardiovascular health. METHODS: A prospective analysis was conducted from January to July 2024, focusing on arterial stiffness parameters in a cohort of students from the Carol Davila University of Medicine and Pharmacy. Participants were categorized as smokers or non-smokers based on self-reported smoking status. The study endpoints included correlations between high pulse wave velocity, elevated peripheral and central systolic blood pressure, increased peripheral and central pulse pressure, and smoking status. These markers were assessed using an arteriograph device measuring the time difference between the initial forward pulse wave and the reflected pulse wave in the brachial artery to indirectly estimate the PWV using oscillometric pulsations. RESULTS: Our investigation, involving 102 young individuals aged 20 to 26 (69 females, 33 males), revealed that smokers exhibited significantly higher average values of arterial stiffness indicators compared to non-smokers. Current smokers had higher mean systolic blood pressure (130.65 vs. 123.05 mmHg), higher mean peripheral pulse pressure (53.19 vs. 45.64 mmHg), higher mean central pulse pressure (33.66 vs. 29.69 mmHg), and higher mean pulse wave velocity (5.27 vs. 5.03 m/s). CONCLUSIONS: The utilization of arterial stiffness markers as predictive tools offers opportunities for personalized treatment strategies, potentially enhancing cardiovascular health outcomes.
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Objective:Wellens syndrome has been described as a clinical and electrocardiographic complex that identifies a subset of patients with unstable angina (UA) at an impending risk of myocardial infarction (MI) and death in studies published almost four decades ago, before the wide use of cardiac biomarkers such as troponins. The clinical implications of Wellens sign in a contemporary cohort of patients with non-ST elevation acute coronary syndromes (NSTEACS) is yet to be defined. Material and methods:We performed a prospective analysis of patients with acute coronary syndrome (ACS) and Wellens sign who underwent coronary angiography between January 2018 and December 2019. Patients follow-up visits were at one month and at six months. Clinical, electrocardiographic, biological and echocardiographic data were recorded at both follow-up visits. Results: A total of 79 patients were included in the statistical analysis, of whom 16 (20.25%) had pure Wellens syndrome (normal myocardial necrosis biomarkers). The prevalence of type A Wellens sign was higher than previously reported (45.6%). The culprit coronary artery was most frequently LAD (49 pts, 62.03%), followed by LM (10 patients, 12.66%), right coronary artery (RCA) (eight pts, 10.13%), instent restenosis (three pts, 3.8%), left circumflex artery (LCX) (two pts, 2.53%) and bypass graft (one pt, 1.27%). Ischaemic reccurence rate within six months was 18,99%. The rate of reccurent percutaneous revascularization procedures was 11.54% and the rate of repeat target vessel revascularization (TVR) was 5.77% at six months. All-cause mortality rate at six months was 7.59%, with 5.06% cardiovascular deaths. Conclusion: Early recognition of subtle ECG changes resembling Wellens sign in patients with chest pain is crucial as it reflects a large area of myocardium at risk. In our study, the culprit coronary artery was most frequently LAD (62.03%), with 36.7% proximal LAD culprit lesion, followed by LM (12.66%). Wellens syndrome should be considered a high risk condition that makes the conventional methods for risk assesment using risk scores unnecessary, useless and potentially deleterious. In our study, according to GRACE 1.0 risk score, 70.89% of patients were in the low risk group (1-108 points, estimated in-hospital death risk < 1%). No patient died during the initial hospitalization. All-cause mortality rate at six months was 7.59%, with 5.06% cardiovascular deaths.
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RATIONALE: Coronary chest pain is usually ischemic in etiology and has various electrocardiographic presentations. Lately, it has been recognized that myocardial bridging (MB) with severe externally mechanical compression of an epicardial coronary artery during systole may result in myocardial ischemia. Such a phenomenon can be associated with chronic angina pectoris, acute coronary syndromes (ACS), coronary spasm, ventricular septal rupture, arrhythmias, exercise-induced atrioventricular conduction blocks, transient ventricular dysfunction, and sudden death. PATIENT CONCERNS: We report the case of a 58-year-old woman presenting with recurrent episodes of constrictive chest pain during exercise within the last 2 weeks. Except for obesity, general and cardiovascular clinical examination on admission were normal. DIAGNOSES: The resting 12 lead electrocardiogram (ECG) revealed changes typically for Wellens syndrome. High-sensitive cardiac troponin I was normal. We established the diagnosis of low-risk non-ST-segment elevation acute coronary syndrome with a Global Registry of Acute Coronary Events risk score of 92 points. INTERVENTIONS: The patient underwent coronary angiography, who showed subocclusive dynamic obstruction of the left anterior descending artery due to MB. OUTCOMES: The patient was managed conservatively. Her hospital course was uneventful and she was discharged on pharmacological therapy (clopidogrel, bisoprolol, amlodipine, atorvastatin, and metformin) with well-controlled symptoms on followup. LESSONS: MB is an unusual cause of myocardial ischemia. Wellens syndrome is an unusual presentation of ACS. We present herein a rare case of Wellens syndrome caused by MB. This case highlights the importance of subtle and frequently overseen ECG findings when assessing patients with chest pain and second, the importance of considering nonatherosclerotic causes for ACS.