Coronary artery diseases (CAD), also known as coronary heart disease (CHD), are the world’s leading cause of death. The basis of coronary artery disease is the narrowing of the heart coronary artery lumen due to atherosclerosis. The use of electronic cigarettes has increased significantly over the years. However, harmful effects of electronic cigarettes are still not firm. The aim of this article is to review the impact of electronic cigarette and its role in the pathogenesis of atherosclerosis from recent studies. The results showed that several chemical compounds, such as nicotine, propylene glycol, particulate matters, heavy metals, and flavorings, in electronic cigarette induce atherosclerosis with each molecular mechanism that lead to atherosclerosis progression by formation of ROS, endothelial dysfunction, and inflammation. Further research is still needed to determine the exact mechanism and provide more clinical evidence.

Background. Although de Winter T-wave electrocardiography pattern is rare, it signifies proximal left anterior descending artery occlusion and is often unrecognized by physicians. The aim of this case report was to highlight the dilemma in the management of a patient with de Winter T-wave pattern in the hospital without interventional cardiology facility. Case Presentation. A 65-year-old male presented with typical chest pain since 2 hours before admission, and ECG showed sinus rhythm of 57 bpm and >1 mm upsloping ST depression with symmetric tall T in lead V_2-3 characteristic of de Winter T-wave ECG pattern. He was given dual antiplatelet therapy, nitrate, statin, and anticoagulant. He refused referral to interventional cardiology available hospital. 3 hours after admission, the electrocardiography transformed into Q-waves consistent with final stages of acute STEMI and ST-segment elevation that barely meets the threshold in the guideline, and thrombolytic was administered and successful. There is a suggestion that de Winter T-wave electrocardiography should be treated as ST-segment myocardial infarction equivalent and should undergo coronary angiography; however, not every hospital has the luxury of interventional cardiology facility. The other modality for reperfusion is thrombolysis; however, without a clear guideline and scarcity of study, we prefer to resort to conservative treatment. “Fortunately,” transformation into ST-segment elevation helps us to determine the course of action which is reperfusion using thrombolytic. Conclusions. de Winter T-wave ECG pattern is not mentioned in any guidelines regarding acute coronary syndromes, and there are no clear recommendations. Physicians in rural area without interventional cardiology facility face a dilemma with the lack of evidence-based guideline. Fibrinolytic may be appropriate in those without contraindications with strong chest pain consistent with acute coronary occlusion, less than 3 hours of symptoms, and convincing de Winter T-wave ECG pattern for a rural non-PCI hospital far away from PCI capable hospital.

Coronary artery ectasia is characterized by an abnormal dilatation of the coronary arteries. Coronary artery ectasia is observed in 3–8% of patients undergoing coronary angiography and sometimes leads to acute coronary syndrome regardless of the presence or absence of coronary stenosis or atrial fibrillation. A 61-year-old Indonesian man presented with typical angina that began 1 week before admission and had worsened 3 hours prior to admission. Accompanying symptoms included dyspnea, nausea, and sweating. He was hemodynamically stable and had a history of tobacco smoking and dyslipidemia. An electrocardiogram showed ST-segment depression and T inversion. Laboratory results showed an international normalized ratio of 1.28. Dual antiplatelet therapy was administered along with fondaparinux, and symptoms were alleviated. Coronary angiography showed an ectatic and turbulent mid-distal right coronary artery and slow flow at the first presentation. There was a patent stent in the proximal-mid left anterior descending coronary artery. This patient had previously presented with recurrent acute coronary syndrome and received two coronary stents for the stenotic vessels. He had right coronary artery ectasia and experienced recurrent acute coronary syndrome. He received dual antiplatelet therapy along with warfarin after stenting of his left anterior descending coronary artery. However, he presented with unstable angina pectoris 7 months before the latest admission and at the latest admission despite a patent stent and no other significant obstructive lesion. The unstable angina pectoris might have been caused by slow flow, microvascular angina caused by small thrombi and/or vasospasm, or epicardial thrombosis at the ectatic coronary artery that dissolved after anticoagulation therapy prior to coronary angiography. Anticoagulant therapy may have a greater benefit than antiplatelet therapy in this patient due to the turbulence and stasis of blood in the ectatic vessel, although coexisting coronary conditions mandated antiplatelet therapy. His international normalized ratio was suboptimal and needed to be improved. Coronary ectasia may play a role in recurrent acute coronary syndrome, and administration of an anticoagulant to prevent acute coronary syndrome in this patient was in accordance with the varying hemodynamic property of coronary artery ectasia.

Moderate intensity exercise is considered as a primary step to prevent coronary artery diseases (CADs) by stimulated FSTL-1 secretion as a novel myokines to improve endothelial cell function, prevent arterial stiffness, or vascular inflammation. This review aims to provide the current evident role of FSTL-1 as a novel myokine secreted during exercise to prevent atherosclerosis progression. A systematic review using databases from (PubMed), ScienceDirect, and The Cochrane Library, was conducted up to October 2021 to identify all the eligible experimental and observational studies that assess how moderate intensity exercises stimulate FSTL-1 secretion to prevent atherosclerosis. Results were described through narrative synthesis of the evidence. From 84 retrieved references, 15 studies met the inclusion criteria and were included in this review. The overall results suggest that exercise or physical activity can stimulate myokines secretion, especially in FSTL-1. FSTL-1 is a myokine or adipokine that plays a potential role in preventing atherosclerosis by various mechanisms such as via improvement of endothelial functions, suppression of smooth muscle cells (SMCs) proliferation, and reduction of arterial thickening. FSTL-1 is a relatively new and less known myokine, but probably holds a key role in assessing how moderate intensity aerobic exercise prevents atherosclerosis progression by preventing endothelial dysfunction, arterial stiffness, or vascular inflammation.

The popularity of the electronic cigarette has soared in the last decades. However, the health effect of smoking electronic cigarettes on the vascular system is unclear. This systematic review examines the electronic cigarettes effect on the vascular system from recent evidence. A systematic search was conducted in MEDLINE (PubMed) database from January 2016 to August 2021 for studies assessing the vascular effect of chronic use of electronic cigarettes on human and animal. The Cochrane Risk of Bias 2, NIH Quality Assessment for Cross-Sectional Study, and SYRCLEs Risk of Bias were used to assess the risk of bias in interventional, observational, and animal study, respectively. A narrative synthesis of evidence is provided to describe results. From 101 retrieved studies related to electronic cigarettes effect on the vascular system, a total of 16 studies are included in this review. The overall results indicated that electronic cigarette use is associated with adverse events in the vascular, including the incident of elevated oxidative stress, endothelial dysfunction, inflammation, arterial stiffness, and the development of atherosclerotic lesion. Further studies should broaden perspectives and reveal more about the mechanism of how electronic cigarettes impact on vascular system.