Numerous randomized controlled trials have investigated the efficacy of optimal medical therapy (OMT) for atherosclerotic cardiovascular disease (ASCVD), specifically chronic coronary syndrome. Mounting evidence has shown that low-density lipoprotein (LDL)-lowering therapy is the cornerstone of OMT and improves the prognosis. Lipoprotein A [Lp(a)], identified in 1963, is an important risk factor for ASCVD independent of other traditional risk factors, including LDL cholesterol. Lp(a) is an apolipoprotein B (apoB)-containing lipoprotein that contains LDL-like particles. Lp(a) has been suggested to be a causal factor for ASCVD, but no substantial evidence supports this because there is currently no medical therapy that specifically reduces Lp(a). However, several novel drugs, including oligonucleotide therapeutics, are currently undergoing clinical trials that may yield the required evidence. This review describes the current understanding and future perspectives of Lp(a), which is currently considered a mere biomarker but can be a novel therapeutic target in the near future.

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The importance of optimal medical therapy for chronic coronary syndrome was demonstrated in the COURAGE and ISCHEMIA trials. Hypertension is an important risk factor for atherosclerotic disease; however, it has not garnered as much attention as low-density lipoprotein cholesterol in coronary artery diseases. Blood pressure contributes significantly to the development of atherosclerosis, an underlying pathological mechanism of chronic coronary syndrome. This is due to shear stress, which causes endothelial dysfunction and angiotensin II-induced intimal smooth muscle cell proliferation. Although the renin-angiotensin system plays an important role in atherosclerosis, the strong expression of angiotensin-converting enzyme in macrophages and angiotensin II type 1 receptors in smooth muscle cells suggests that this pathway may be involved in different local pathologies. Furthermore, an imbalance between myocardial oxygen demand and supply contributes to chronic coronary syndromes. An elevated systolic blood pressure also has a significant impact on increased myocardial oxygen consumption. Therefore, adequate blood pressure reduction is important to prevent the development of chronic coronary syndrome. Percutaneous coronary intervention, which significantly contributes to the treatment of chronic coronary syndrome, requires aggressive antithrombotic therapy. Although antithrombotic therapy has significantly increased the success rate, it is also associated with an increase in the incidence of serious adverse bleeding events. A bleeding with antithrombotic therapy study conducted in Japan reported that a robust antihypertensive regimen could reduce the incidence of intracranial hemorrhaging. Percutaneous coronary intervention for chronic coronary syndrome is an elective procedure that should be performed only after adequate blood pressure reduction has been achieved.

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Anastomotic quality is directly associated with clinical outcomes of patients after coronary artery bypass grafting (CABG). Early and late graft failure are potentially fatal complications that can cause refractory angina, myocardial infarction, and arrhythmias. Hence, intraoperative graft assessment is of paramount importance in detecting stenotic anastomoses and ensuring the future graft function. Transit-time flow measurement (TTFM) is a less invasive and frequently used technique for intraoperative graft assessment during CABG. Previous studies have indicated that TTFM provides great benefits for patients in intraoperatively detecting stenotic anastomoses and in avoiding unnecessary postoperative complications. Accordingly, current clinical guidelines recommend routine intraoperative graft flow measurements during CABG. However, the interpretation of composite or sequential grafting by TTFM to predict the risk of graft failure remains controversial. Additionally, the TTFM prognostic value demonstrated lower accuracy in detecting anastomotic stenosis in patients with saphenous vein grafts than in patients with intrathoracic artery grafts. This clinically focused review of TTFM assessment of CABG revealed the clinical advances acquired with TTFM, which were diagnostically used in the detection of anastomotic stenosis in previously published studies. We provide a systematic overview of the evidence and considerations regarding the following topics: general principles of TTFM, intraoperative acquisition protocol, effects of TTFM on postoperative clinical outcomes, recommended cutoff values for each parameter, and the influence of graft type on the diagnostic value of TTFM.

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Hybrid coronary revascularization (HCR) is an emerging approach for multivessel coronary artery disease that combines the excellent long-term outcomes of surgery with the faster recovery and reduced short-term complications of percutaneous coronary intervention. This review addresses the features of HCR, including patient selection and effectiveness.

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Objectives: We retrospectively analyzed the usefulness and safety of intracoronary acetylcholine (ACH) 80 µg in the right coronary artery (RCA) for vasoreactivity testing compared with a maximum ACH dose of 50 µg.
Methods: We recruited 1,351 patients with angina-like chest pain who underwent intracoronary ACH testing in the RCA, including 673 patients with a maximum ACH dose of 50 µg and 678 patients with a maximum ACH dose of 80 µg. ACH was injected into the RCA at incremental doses of 20/50/80 µg. Positive spasm was defined as ≥ 90% stenosis, usual chest pain, or ischemic electrocardiogram (ECG) changes.
Results: The incidence of coronary constriction ≥ 90%, usual chest pain, and ischemic ECG changes with a maximum ACH dose of 50 µg was markedly higher than that with a maximum ACH dose of 80 µg. In 38 variant angina patients with ST elevation in the inferior leads, a maximum dose of intracoronary ACH 50 µg and ACH 80 µg but not 50 µg disclosed coronary constriction in 21 and 9 patients, respectively, whereas intracoronary ergonovine provoked coronary constriction in 4 patients who had no coronary constriction by intracoronary ACH 50 or 80 µg. Major complications during ACH testing in the RCA did not differ markedly between the maximum ACH 50 and 80 µg groups (2.38% vs. 1.33%, p = 0.152), whereas paroxysmal atrial fibrillation was significantly higher in the maximum ACH 50 µg group than in the maximum ACH 80 µg group (25% vs. 14%, p < 0.001).
Conclusions: Intracoronary ACH 80 µg in the RCA is useful and safe for vasoreactivity testing when intracoronary ACH 50 µg does not provoke spasm.

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