Glucagon-like peptide-1 (GLP-1) is an incretin hormone that has a wide range of effects on glucose metabolism and cardiovascular function (e.g., improving insulin sensitivity, reduction in appetite, modulation of heart rate, blood pressure and myocardial contractility). Metabolic syndrome (MetS) is associated with an increased risk of developing atherosclerotic cardiovascular diseases. Novel glycemic control drugs, the dipeptidyl-peptidase-4 (DPP-4) inhibitors, work by inhibiting the inactivation of incretin hormones, GLP-1 and glucose-dependent insulinotropic polypeptide (GIP). In spite of good effects of these drugs in diabetic patients, circulating levels of incretins and their role in MetS are largely unknown.

Herpes zoster, induced by the reactivation of the varicella-zoster virus (VZV), is a unilaterally distributed vesicular rash that can cause multiple complications. VZV not only causes neurological problems, including postherpetic neuralgia and ocular zoster, but also causes inflammatory vasculopathy and increases the incidence of hemorrhagic or ischemic complications. Therefore, understanding the association between the development of herpes zoster and the subsequent occurrence of acute stroke or cardiovascular diseases, including myocardial infarction and heart failure, is of great interest. Conversely, many risk factors are involved in the development of herpes zoster. Recently, it has become clear that aging, insufficient immune function, and diseases related to lifestyle habits (for example, stroke and cardiovascular disease), can trigger the onset of herpes zoster. Preventing the onset of herpes zoster, which substantially reduces quality of life, will lead to lower medical costs for countries and extend healthy life expectancy for general populations. Thus, because herpes zoster is a vaccine-preventable disease, active vaccination is recommended for high-risk groups. This review summarizes the association between herpes zoster and cardiovascular disease and vaccination against herpes zoster as a useful disease management and prevention measure for cardiovascular disease.

Metabolic syndrome (MetS) is associated with an increased risk of the development of atherosclerotic cardiovascular disease (CVD). Interleukin-18 (IL-18), which is a pleiotropic proinflammatory cytokine with important regulatory functions in the innate immune response system, plays a crucial role in vascular pathologies. IL-18 is also a predictor of cardiovascular death in patients with CVD and is involved in atherosclerotic plaque destabilization.

The risk of cardiovascular complication in a diabetes patient is similar to that in a nondiabetic patient with a history of myocardial infarction. Although intensive control of glycemia achieved by conventional antidiabetic agents decreases microvascular complications such as retinopathy and nephropathy, no marked effect has been reported on macrovascular complications or all-cause mortality. Evidence from VADT, ACCORD, and ADVANCE would suggest that glycemic control has little effect on macrovascular outcomes. Moreover, in the case of ACCORD, intensive glycemic control may be associated with an increased risk of mortality. There is sufficient evidence that suggests that postprandial hyperglycemia may be an independent risk factor for cardiovascular disease in diabetes patients. However, there are no prospective clinical trials supporting the recommendation that lowering postprandial blood glucose leads to lower risk of cardiovascular outcomes. Mitiglinide is a short-acting insulinotropic agent used in type 2 diabetes treatment. It has a rapid stimulatory effect on insulin secretion and reduces postprandial plasma glucose level in patients with type 2 diabetes. Because of its short action time, it is unlikely to exert adverse effects related to hypoglycemia early in the morning and between meals. Mitiglinide reduces excess oxidative stress and inflammation, plays a cardioprotective role, and improves postprandial metabolic disorders. Moreover, mitiglinide add-on therapy with pioglitazone favorably affects the vascular endothelial function in type 2 diabetes patients. These data suggest that mitiglinide plays a potentially beneficial role in the improvement of postprandial hyperglycemia in type 2 diabetes patients and can be used to prevent cardiovascular diseases. Although the results of long-term, randomized, placebo-controlled trials for determining the cardiovascular effects of mitiglinide on clinical outcomes are awaited, this review is aimed at summarizing substantial insights into this topic.

Ezetimibe (Zetia^®) is a potent inhibitor of cholesterol absorption that has been approved for the treatment of hypercholesterolemia. Statin, an inhibitor of cholesterol synthesis, is the first-choice drug to reduce low-density lipoprotein-cholesterol (LDL-C) for patients with hypercholesterolemia, due to its strong effect to lower the circulating LDL-C levels. Because a high dose of statins cause concern about rhabdomyolysis, it is sometimes difficult to achieve the guideline-recommended levels of LDL-C in high-risk patients with hypercholesterolemia treated with statin monotherapy. Ezetimibe has been reported to reduce LDL-C safely with both monotherapy and combination therapy with statins. To investigate the effect of ezetimibe as "add-on" therapy to statin on hypercholesterolemia, we examined biomarkers and vascular endothelial function in 14 patients with hypercholesterolemia before and after the 22-week ezetimibe add-on therapy. Ezetimibe add-on therapy reduced LDL-C by 24% compared with baseline (p < 0.005), with 13 patients (93%) reaching their LDL cholesterol goals. Of the Ezetimibe add-on therapy significantly improved not only LDL-C, high-density lipoprotein-cholesterol (HDL-C), and apolipoprotein (apo)B levels, but also reduced levels of triglyceride (TG), the ratio of LDL/HDL-C, the ratio of apoB/apoA-I, and a biomarker for oxidative stress (d-ROMs). Furthermore, ezetimibe add-on therapy improved vascular endothelial function in high-risk patients with hypercholesterolemia. In conclusion, ezetimibe as add-on therapy to statin might be a therapeutic good option for high-risk patients with atherosclerosis.

Natural disasters, such as floods and landslides caused by heavy rainfall, earthquakes, and tsunamis, can induce stress, which may contribute to the onset and aggravation of various cardiovascular diseases. The circulatory system is most susceptible to the effects of stress, and stress-related cardiovascular diseases, such as Takotsubo cardiomyopathy, pulmonary thromboembolism, hypertension, stroke triggered by increased blood pressure, and acute myocardial infarction, can occur during natural disasters. The risk of developing angina pectoris, arrhythmia, sudden cardiac death, and heart failure increases rapidly and can persist for several months. Moreover, treating cardiovascular diseases is essential during the acute phase, and continuous disease management is necessary during the chronic phase. However, disaster medical care for the victims must be given priority during natural disasters, which may cause a delay in diagnosis or access to necessary treatment for pre-existing medical conditions that could worsen or may cause death in patients with cardiovascular diseases. In this review, we summarize the predisposing factors for cardiovascular diseases that have been obtained through disasters such as major earthquakes and provide potential insights to help medical staff prevent the onset and aggravation of cardiovascular diseases during disasters.