Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.

Heart failure is a complex syndrome responsible for high rates of death and hospitalization. Ischemic heart disease is one of the most frequent causes of heart failure and it is normally attributed to coronary artery disease, defined by the presence of one or more obstructive plaques, which determine a reduced coronary blood flow, causing myocardial ischemia and consequent heart failure. However, coronary obstruction is only an element of a complex pathophysiological process that leads to myocardial ischemia. In the literature, attention paid to the role of microcirculation, in the pathophysiology of ischemic heart disease and heart failure, is growing. Coronary microvascular dysfunction determines an inability of coronary circulation to satisfy myocardial metabolic demands, due to the imbalance of coronary blood flow regulatory mechanisms, including ion channels, leading to the development of hypoxia, fibrosis and tissue death, which may determine a loss of myocardial function, even beyond the presence of atherosclerotic epicardial plaques. For this reason, ion channels may represent the link among coronary microvascular dysfunction, ischemic heart disease and consequent heart failure.

Advanced heart failure (AdHF) represents a challenging aspect of heart failure patients. Because of worsening clinical symptoms, high rates of re-hospitalization and mortality, AdHF represents an unstable condition where standard treatments are inadequate and additional interventions must be applied. A heart transplant is considered the optimal therapy for AdHF, but the great problem linked to the scarcity of organs and long waiting lists have led to the use of mechanical circulatory support with ventricular-assist device (VAD) as a destination therapy. VAD placement improves the prognosis, functional status, and quality of life of AdHF patients, with high rates of survival at 1 year, similar to transplant. However, the key element is to select the right patient at the right moment. The complete assessment must include a careful clinical evaluation, but also take into account psychosocial factors that are of crucial importance in the out-of-hospital management. It is important to distinguish between AdHF and end-stage HF, for which advanced therapy interventions would be unreasonable due to severe and irreversible organ damage and, instead, palliative care should be preferred to improve quality of life and relief of suffering. The correct selection of patients represents a great issue to solve, both ethically and economically.

Introduction. Despite a successful percutaneous coronary intervention (PCI), several studies reported that the recurrence of angina after revascularization, even complete, is a particularly frequent occurrence in the first year after PCI. Methods. The aim was to evaluate the efficacy of treatment with ranolazine in addition to conventional anti-ischemic therapy in patients who underwent coronary angiography for persistent/recurrent angina after PCI and residual ischemia only due to small branches not suitable for further revascularization. Forty-nine consecutive patients were included in our registry, adding the ranolazine (375 mg b.i.d) to optimal medical therapy (OMT). The Exercise ECG Test (EET) was performed in all patients before to start the therapy (baseline BL) and at 30 days (T1) after enrollment. Results. The average duration of the exercise was increased after the therapy with ranolazine comparing to baseline (RG 9’1” ± 2’ versus BL 8’10” ± 2’, p = 0.01). Seven (14.3%) patients after receiving ranolazine had not crossed the threshold of six minutes (75 watts) compared to 20 (40.8%) of BL (p = 0.0003). Stress angina appeared more frequently at BL than at 30 days (T1 4.1% versus BL 16.3%, p = 0.04) as well as exercise-induced arrhythmias (BL 30.6% versus T1 14.3%, p = 0.05). Conclusions. The addition of ranolazine to standard anti-ischemic therapy showed a significant improvement in EET results after one month of therapy, including reduced exercise angina, increased exercise tolerance, and reduced exercise arrhythmias.

Coronary artery aneurysms (CAAs) are uncommon but significant cardiovascular abnormalities characterized by an abnormal increase in vascular diameter. CAAs are classified based on their shape as either saccular or fusiform, and their causes can range from atherosclerosis, Kawasaki disease, to congenital and iatrogenic factors. CAAs often present asymptomatically, but when symptoms occur, they can include angina, myocardial infarction, or even sudden cardiac death due to intravascular thrombosis involving the CAA. Diagnosis is typically confirmed through coronary angiography, though CT and other imaging techniques can provide additional details. The management of CAAs is variable depending on their size, location, and the presence of symptoms or complications. Treatment options include medical therapy, percutaneous coronary intervention (PCI), or surgical approaches. In this paper, we describe the case report of a 79-year-old male who presented with palpitations and was diagnosed with a right coronary artery aneurysm, and a review of the literature is delineated, underscoring the importance of individualized treatment strategies for CAAs.