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The infection caused by the Human Immunodeficiency Virus (HIV) has spread rapidly across the globe, assuming the characteristics of an epidemic in some regions. Thanks to the introduction of antiretroviral therapy into routine clinical practice, there was a considerable breakthrough in the treatment of HIV, that is now HIV is potentially well-controlled even in low-income countries. To date, HIV infection has moved from the group of life-threatening conditions to the group of chronic and well controlled ones and the quality of life and life expectancy of HIV + people, with an undetectable viral load is closer to that of an HIV - people. However, unsolved issues still persist. For example: people living with HIV are more prone to the age-related diseases, especially atherosclerosis. For this reason, a better understanding of the mechanisms of HIV-associated destabilization of vascular homeostasis seems to be an urgent duty, that may lead to the development of new protocols, bringing the possibilities of pathogenetic therapies to a new level. The purpose of the article was to evaluate the pathological aspects of HIV-induced atherosclerosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known any competing financial interests or personal relationships that could have appeared to influence the work reported in this statement., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: There is limited information available regarding evidence of ischemia with no obstructive coronary arteries (INOCA) and quality of life., Purpose: To determine associations between INOCA and self-reported physical, social, and mental health., Methods: We conducted a survey of all members (n = 1579) of the INOCA International patient support group. Current self-reported diagnosis and health measures were collected. Functional capacity was retrospectively estimated using the Duke Activity Status Index (DASI), assessing levels of activities performed prior and after symptom onset., Results: A total of 297 (20.8% response rate, 91% women) reported symptoms of chest pain, pressure, or discomfort in 92.9%. Overall, 34.4% were living with symptoms for ≥3 years before an INOCA diagnosis, and 77.8% were told their symptoms were not cardiac. Estimated functional capacity was higher prior to compared to after symptom onset (8.6 ± 1.8 METs vs 5.6 ± 1.8 METs; P < 0.0001). Most respondents reported an adverse impact of symptoms on their home life (80.5%), social life (80.1%), mental health (70.4%), outlook on life (69.7%), sex life (55.9%), and their partner/spouse relationship (53.9%), while approximately three-quarters reduced their work hours or stopped work completely, 47.5% retired early, and 38.4% applied for disability., Conclusions: INOCA symptoms are associated with adverse physical, mental and social health quality of life. Increased patient awareness, physician recognition and diagnosis, and clinical trials are needed to develop evidence-based guidelines for this increasingly recognized cardiovascular disorder., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Both the latest European guidelines on chronic coronary syndromes and the American guidelines on chest pain have underlined the importance of noninvasive imaging to select patients to be referred to invasive angiography. Nevertheless, although coronary stenosis has long been considered the main determinant of inducible ischemia and symptoms, growing evidence has demonstrated the importance of other underlying mechanisms (e.g., vasospasm, microvascular disease, energetic inefficiency). The search for a pathophysiology-driven treatment of these patients has therefore emerged as an important objective of multimodality imaging, integrating "anatomical" and "functional" information. We here provide an up-to-date guide for the choice and the interpretation of the currently available noninvasive anatomical and/or functional tests, focusing on emerging techniques (e.g., coronary flow velocity reserve, stress-cardiac magnetic resonance, hybrid imaging, functional-coronary computed tomography angiography, etc.), which could provide deeper pathophysiological insights to refine diagnostic and therapeutic pathways in the next future., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Clinical outcomes of stable angina patients treated according to guidelines recommendations (medical therapy first, selective revascularization in high risk or unresponsive patients) are not fully known., Methods and Results: Eight hundred thirty-three patients with newly diagnosed, stable angina were enrolled in a prospective, observational, nationwide registry and followed for 1 year. Symptoms and quality of life were evaluated with the CCS angina grading, with a self-assessment scale and with the SAQ-7. A composite end-point of MACEs (all-cause death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for unstable angina) at 1 year was considered. Upon enrollment, all patients were prescribed guidelines directed medical therapy. After one month of therapy, angina relieved or improved in 47% of the overall population. Patients in CCS class I significantly increased from 28.4% at enrollment to 67.1% at 12 months, and the SAQ-7 score from 58.4 ± 20 to 85.9 ± 14. The rate of MACEs was low (2.9%) in the overall population. After one month of medical therapy, 40.6% of patients were referred for coronary angiography and revascularization for resistant symptoms (invasive strategy). Among these, 38.2% had normal coronary arteries and 47% actually underwent revascularization. No difference between invasive and medical groups was found at 12 months in symptoms, quality of life and MACEs, except for a greater improvement in self-assessed symptoms in the invasive group. Combined medical and invasive strategies left 28.5% of patients still symptomatic at the end of the study., Conclusions: The study confirms the efficacy and safety of a tailored approach to stable angina, as recommended by guidelines, with medical therapy first followed by selective revascularization when needed., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)

Although current guidelines on the management of stable coronary artery disease acknowledge that multiple mechanisms may precipitate myocardial ischemia, recommended diagnostic, prognostic and therapeutic algorithms are still focused on obstructive epicardial atherosclerotic lesions, and little progress has been made in identifying management strategies for non-atherosclerotic causes of myocardial ischemia. The purpose of this consensus paper is three-fold: 1) to marshal scientific evidence that obstructive atherosclerosis can co-exist with other mechanisms of ischemic heart disease (IHD); 2) to explore how the awareness of multiple precipitating mechanisms could impact on pre-test probability, provocative test results and treatment strategies; and 3) to stimulate a more comprehensive approach to chronic myocardial ischemic syndromes, consistent with the new understanding of this condition., Competing Interests: Declaration of competing interest The authors report no relationships that could be construed as a conflict of interest., (Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Abnormalities of myocardial energy metabolism appear as a common background of the two major cardiac disorders: ischemic heart disease (IHD) and heart failure (HF). Myocardial ischemia has been recently conceived as a multifaceted syndrome that can be precipitated by a number of mechanisms including metabolic abnormalities. HF is a progressive disorder characterised by a complex interaction of haemodynamic, neurohormonal and metabolic disturbances. HF may further promote metabolic changes, generating a vicious cycle. Thus, targeting cardiac metabolism in IHD patients may prevent the deterioration of left ventricular function, stopping the progression to HF. For these reasons, several studies have explored the potential benefits of trimetazidine (TMZ), an inhibitor of free fatty acids oxidation that shifts cardiac and muscle metabolism to glucose utilization. Because of its mechanism of action, TMZ has been found to provide a cardioprotective effect in patients with angina, diabetes mellitus, and left ventricular (LV) dysfunction, and those undergoing revascularization procedures, without relevant side effects. In addition, the lack of interference with heart rate, arterial pressure, and most of frequent comorbidities, makes TMZ an attractive option for patients and clinicians as well. The impact of TMZ on long term mortality and morbidity in ischemic syndromes and in heart failure need to be conclusively confirmed in properly designed RCT., (Copyright © 2019. Published by Elsevier B.V.)

Background: The cornerstone of the treatment of patients affected by stable angina is based on drugs administration classified as first (beta-blockers, calcium channel blockers, short acting nitrates) or second line treatment (long-acting nitrates, ivabradine, nicorandil, ranolazine and trimetazidine). However, few data on comparison between different classes of drugs justify that one class of drugs is superior to another., Methods: We performed a systematic review of the literature following PRISMA guidelines., Inclusion Criteria: i) paper published in English; ii) diagnosis of stable coronary disease; iii) randomized clinical trial; iv) comparison of two anti-angina drugs; v) a sample size >100 patients; vi) a follow-up lasting at least 2 weeks; vii) paper published after 1999, when a meta-analysis of trials comparing beta-blockers, calcium antagonists, and nitrates for stable angina of Heidenreich et al. was published., Outcome: to establish whether the categorization in first and second line antianginal treatment is scientifically supported., Results: Eleven trials fulfilled inclusion criteria. The results show that there is a paucity of data comparing the efficacy of antianginal agents. The little data available show that there are not compounds superior to others in terms of improvement in exercise test duration, frequency of anginal attacks, need for sub-lingual nitroglycerin., Conclusion: The categorization of antianginal drug in first and second line is not confirmed., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: In RCTs about revascularization, the terms "coronary artery disease" and "ischemic heart disease" are sometimes used interchangeably. This can create confusion concerning inclusion and exclusion criteria, which may lead to uncertain results., Objective: Our purpose is to investigate whether the study populations in randomized controlled trials (RCTs) which compared percutaneous coronary revascularization to medical therapy for stable ischemic heart disease specifically enrolled patients with demonstrable ischemia, and how many patients were included in trials with evidence of coronary atherosclerosis but without evidence of ischemia., Methods: Trial published data were obtained from ACME I, ACME II, RITA I, RITA II, MASS I, MASS II, AVERT, ACIP, COURAGE and FAME2. Published data were used to calculate the number of patients included in the trials with a negative stress test but significant coronary artery stenosis and the number of patients excluded from the trials with a positive stress test or angina, but without significant coronary artery stenosis at the time of angiography., Results: A total of 196,433 patients were screened between 1998 and 2011. Overall about 30% of patients were excluded if they did not meet the angiographic criteria, even though the presence of inducible ischemia or angina, and, about 20% of patients were included without inducible ischemia., Conclusion: RCTs have contributed to the confusion between coronary artery disease and ischemic heart disease. This may limit the ability to interpret the results and apply them in practice., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Noninvasive stress tests play a determinant role in the initial management of patients with chronic angina. Nonetheless, their use in the same patient population is considered inappropriate within 2 years after percutaneous coronary intervention (PCI). Indeed, early abnormal results correlate less well with angiographic control and are attributed to a number of confounding factors. We prospectively assessed prevalence and impact on the quality of life of abnormal stress test results in a highly selected patient population., Methods: Patients with no cardiac comorbidities who underwent successful and complete PCI with stenting for typical angina and had an abnormal exercise stress test (EST) under guideline-directed medical treatment were administered the Seattle Angina Questionnaire (SAQ). Clinical evaluation, EST, and the SAQ were repeated at 1, 6, and 12 months after the index PCI., Results: One hundred ninety-eight patients qualified and were included in the study (mean age, 64 years; 79% men). Although the majority had normal EST results or an increased threshold to angina, at 1 month after the index PCI, 29% of patients still had an abnormal result. At 6 and 12 months, 31% and 29% of patients had abnormal results, respectively. Quality-of-life assessment by the SAQ showed consistent results, with persistent angina in one third of patients. Control angiography documented a critical lesion, attributable to in-stent coronary restenosis, in only 8% of patients., Conclusions: When stress testing is systematically performed after PCI, the prevalence of abnormal results is high and is associated with impaired quality of life. Prognostic significance along with the underlying pathophysiological mechanisms of such findings should be investigated., (Copyright © 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

The purpose of this study was to assess clinical correlates of the 'no reflow' phenomenon in 21 consecutive patients with acute myocardial infarction and complete occlusion of the infarct related artery (TIMI 0 flow) that underwent successful direct PTCA. After successful recanalization, 11 patients (group I) maintained TIMI 3 flow and ten patients presented with the 'no reflow' phenomenon (Group II). New Q wave on the surface ECG appeared in six patients in group I and in nine patients in group II (P=NS), clinical and radiologic signs of cardiac failure were detected in two patients in group I and in seven patients in group II (P<0.03). Early recurrence of ischemia was reported in three patients of group II but not in group I (P=NS). We conclude that the 'no reflow' phenomenon occurs in about half the cases of direct PTCA for complete occlusion and predicts adverse clinical events.

Functional factors are known to precipitate ischemic episodes at rest in variant angina, but the role of fixed coronary lesions is still debated. The prevalence, extent, severity and prognostic implications of organic coronary stenoses in variant angina were evaluated in 162 patients with transient ST segment elevation documented during hospitalization. Seventy-eight patients had normal coronary arteries or single-vessel coronary lesions (group 1) and 84 patients had multivessel coronary stenoses (group 2). Both groups were followed up for 82 +/- 41 months. Angiographically normal coronary arteries were observed in only 11 patients (7%). In 59 patients with single-vessel coronary stenoses, the internal luminal diameter was reduced by 51 +/- 12%. There were 20 deaths (16 from cardiac causes) during the 5-year follow-up. Kaplan-Meier survival analysis revealed a significantly lower 5-year survival rate in group 2 (80.1%) compared to group 1 (94.6%, p = 0.006 by Mantel-Haenszel test). If only cardiac causes of death were considered, the 5-year survival rate was still lower in group 2 (84.0%) than in group 1 (97.1%, p = 0.004). Considering both revascularized patients and those treated medically for the entire duration of the follow-up, the survival rate was significantly lower in group 2 than in group 1. Finally, the extent of coronary lesions was an independent predictor of survival by Cox multivariate regression analysis. Organic coronary stenoses are frequent in patients with variant angina and are important for the long-term prognosis.

Early administration of thrombolytic agents in acute myocardial infarction lowers mortality and preserves left ventricular function. Currently, only one third of infarct patients receive this treatment, the vast majority being excluded because of restrictive criteria and delayed hospital admission. When correctly administered, thrombolytic therapy achieves reperfusion in 50-85% of occluded vessels. Five to 15% of these initially recanalized vessels eventually reocclude. Possible mechanisms of failure of thrombolytic therapy to induce stable coronary reperfusion include thrombus formation during thrombolysis, platelet activation by thrombolysis, fibrin deposition during thrombolysis, and resistance to thrombolysis. Bleeding complications including intracranial haemorrhage remain a major complication. New therapeutic regimens, new thrombolytic agents and more effective anti-thrombotic drugs, together with intervention strategies that anticipate the time of treatment, promise a significant increase of the overall benefits obtainable with thrombolysis in acute myocardial infarction.

In this report we show that human endothelial cells (EC) can be detected in circulating blood by means of the EC-specific monoclonal antibody (MoAb) designated as CLB-HEC 19 and expressed quantitatively as number of cells per milliliter of whole blood. We first developed a method that was able to recover cultured human EC added to whole blood by Percoll density gradient centrifugation. The final recovery of the EC was 91.6% (SE = 0.65%). The EC were identified in the gradient subfractions by indirect immunofluorescence with the MoAb CLB-HEC 19. This method was then applied to the separation and characterization of EC or EC remnants from the whole arterial and venous blood taken from two groups of patients subjected to heart catheterization. Firstly, a preliminary blood screening of random samples was performed in a group of eight patients (group I) using a scoring evaluation for the presence of EC and the results were expressed as positivity index. Secondly, the complete blood screening of a group of ten patients (group II) was performed for the detection of immunofluorescent cells and the results were expressed as number of EC per milliliter of whole blood. Our results show in both group I and II a significant presence of EC in the blood after catheterization compared with their basal values. The minimal detectable concentration of EC was 0.06 cells/mL (SE = 0.057) of whole blood. We consider this technique as a suitable clinical test for the detection of EC injury in cardiovascular pathology.

In view of the possibility that the mechanism of mitral regurgitation following premature ventricular contractions may contribute to the understanding of mitral regurgitation in clinically important causes of nonrheumatic mitral insufficiency, we studied 320 premature ventricular contractions in eight dogs. Since the papillary muscle is an important component of the mitral valvular complex, the extent and course of lengthening and shortening of the papillary muscle was investigated with ultrasonic crystals implanted within the anterolateral papillary muscle. Lengthening and shortening of a segment of the free wall of the left ventricle was measured simultaneously with identical crystals in three dogs. During sinus rhythm, lengthening of the papillary muscle always began well before the onset of isovolumic contraction of the left ventricle and continued throughout isovolumic contraction, indicating that lengthening occurred during closure of the mitral valve. When lengthening was prevented by premature ventricular contractions, left atrial v waves occurred. These observations indicate that lengthening of the papillary muscle during the latter part of diastole is required for proper closure of the mitral valve and that inadequate lengthening can result in mitral regurgitation.

Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.