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Autoimmune rheumatic diseases (ARDs) are a heterogeneous group of disorders characterized by an inappropriate immune reactivity against different body tissues. Patients affected by ARDs present increased cardiovascular morbidity and mortality, which significantly impacts long-term prognosis. Endothelial dysfunction, inflammation, oxidative stress, and autoimmunity are strictly involved in atherosclerosis progression and coronary microvascular dysfunction (CMD), both of which contribute to increased cardiovascular risk. CMD represents the inability of the coronary microvasculature to respond with vasodilation to increased cardiac metabolic demands and can be assessed by non-invasive and invasive imaging tests. Coronary flow velocity reserve assessed by echocardiography has been demonstrated to accurately identify ARDs patients with CMD. However, stress cardiac magnetic resonance (CMR) accurately assesses myocardial ischemia, perfusion, and viability in ARDs patients. The myocardial perfusion reserve index (MPRI) is a robust semiquantitative imaging marker that represents the vasodilatory capacity of the coronary microcirculation in response to a vasodilator stress. In the absence of significant coronary stenosis, ARDs patients revealed a reduced MPRI in comparison with the general population, regardless of the presence of myocardial fibrosis. Identification of CMD in asymptomatic patients could be crucial to precociously start targeted medical therapy, avoiding major adverse cardiac events in this clinical setting. This review aims to summarize the current evidence regarding CMD in ARDs patients, focusing on the role of stress CMR and the promising myocardial perfusion analysis.

Acute hyperglycemia is a transient increase in plasma glucose level (PGL) frequently observed in patients with ST-elevation myocardial infarction (STEMI). The aim of this review is to clarify the molecular mechanisms whereby acute hyperglycemia impacts coronary flow and myocardial perfusion in patients with acute myocardial infarction (AMI) and to discuss the consequent clinical and prognostic implications. We conducted a comprehensive literature review on the molecular causes of myocardial damage driven by acute hyperglycemia in the context of AMI. The negative impact of high PGL on admission recognizes a multifactorial etiology involving endothelial function, oxidative stress, production of leukocyte adhesion molecules, platelet aggregation, and activation of the coagulation cascade. The current evidence suggests that all these pathophysiological mechanisms compromise myocardial perfusion as a whole and not only in the culprit coronary artery. Acute hyperglycemia on admission, regardless of whether or not in the context of a diabetes mellitus history, could be, thus, identified as a predictor of worse myocardial reperfusion and poorer prognosis in patients with AMI. In order to reduce hyperglycemia-related complications, it seems rational to pursue in these patients an adequate and quick control of PGL, despite the best pharmacological treatment for acute hyperglycemia still remaining a matter of debate.

Background The left ventricular remodeling (LVR) process has limited the effectiveness of therapies after myocardial infarction. The relationship between autoantibodies activating AT1R‐AAs (angiotensin II receptor type 1‐AAs) and ETAR‐AAs (autoantibodies activating endothelin‐1 receptor type A) with myocardial infarction has been described. Among patients with ST‐segment–elevation myocardial infarction, we investigated the relationship between these autoantibodies with LVR and subsequent major adverse cardiac events. Methods and Results In this prospective observational study, we included 131 patients with ST‐segment–elevation myocardial infarction (61±11 years of age, 112 men) treated with primary percutaneous coronary intervention. Within 48 hours of admission, 2‐dimensional transthoracic echocardiography was performed, and blood samples were obtained. The seropositive threshold for AT1R‐AAs and ETAR‐AAs was >10 U/mL. Patients were followed up at 6 months, when repeat transthoracic echocardiography was performed. The primary end points were LVR, defined as a 20% increase in left ventricular end‐diastolic volume index, and major adverse cardiac event occurrence at follow‐up, defined as cardiac death, nonfatal re‐myocardial infarction, and hospitalization for heart failure. Forty‐one (31%) patients experienced LVR. The prevalence of AT1R‐AAs and ETAR‐AAs seropositivity was higher in patients with versus without LVR (39% versus 11%, P

Objective. We studied the prevalence and major predisposing factors of permanent atrial fibrillation (PAF) in a population of hypertensive post-menopausal (HPMW) women. Materials and Methods. We enrolled 125 consecutive HPMW with PAF, 125 HPMW in sinus rhythm were the control group (CG). Women with valvular heart disease, coronary artery disease, WPW syndrome, left ventricular (LV) ejection fraction

Heart transplantation (HT) is the established treatment for end-stage heart failure, significantly enhancing patients’ survival and quality of life. To ensure optimal outcomes, the routine monitoring of HT recipients is paramount. While existing guidelines offer guidance on a blend of invasive and non-invasive imaging techniques, certain aspects such as the timing of echocardiographic assessments and the role of echocardiography or cardiac magnetic resonance (CMR) as alternatives to serial endomyocardial biopsies (EMBs) for rejection monitoring are not specifically outlined in the guidelines. Furthermore, invasive coronary angiography (ICA) is still recommended as the gold-standard procedure, usually performed one year after surgery and every two years thereafter. This review focuses on recent advancements in non-invasive and contrast-saving imaging techniques that have been investigated for HT patients. The aim of the manuscript is to identify imaging modalities that may potentially replace or reduce the need for invasive procedures such as ICA and EMB, considering their respective advantages and disadvantages. We emphasize the transformative potential of non-invasive techniques in elevating patient care. Advanced echocardiography techniques, including strain imaging and tissue Doppler imaging, offer enhanced insights into cardiac function, while CMR, through its multi-parametric mapping techniques, such as T1 and T2 mapping, allows for the non-invasive assessment of inflammation and tissue characterization. Cardiac computed tomography (CCT), particularly with its ability to evaluate coronary artery disease and assess graft vasculopathy, emerges as an integral tool in the follow-up of HT patients. Recent studies have highlighted the potential of nuclear myocardial perfusion imaging, including myocardial blood flow quantification, as a non-invasive method for diagnosing and prognosticating CAV. These advanced imaging approaches hold promise in mitigating the need for invasive procedures like ICA and EMB when evaluating the benefits and limitations of each modality.

BackgroundDistinct contributions by functional or structural alterations of coronary microcirculation in heart transplantation (HT) and their prognostic role have not been fully elucidated. We aimed to identify the mechanisms of coronary microvascular dysfunction (CMD) in HT and their prognostic implications.Methods134 patients, surviving at least 5 years after HT, without evidence of angiographic vasculopathy or symptoms/signs of rejection were included. 50 healthy volunteers served as controls. All underwent the assessment of rest and hyperemic coronary diastolic peak flow velocity (DPVr and DPVh) and coronary flow velocity reserve (CFVR) and its inherent companion that is based on the adjusted quadratic mean: CCFVR = √{(DPVr)2 + (DPVh)2}. Additionally, basal and hyperemic coronary microvascular resistance (BMR and HMR) were estimated.ResultsBased on CFVR and DPVh, HT patients can be assigned to four endotypes: endotype 1, discordant with preserved CFVR (3.1 ± 0.4); endotype 2, concordant with preserved CFVR (3.4 ± 0.5); endotype 3, concordant with impaired CFVR (1.8 ± 0.3) and endotype 4, discordant with impaired CFVR (2.0 ± 0.2). Intriguingly, endotype 1 showed lower DPVr (p < 0.0001) and lower DPVh (p < 0.0001) than controls with lower CFVR (p < 0.0001) and lower CCFVR (p < 0.0001) than controls. Moreover, both BMR and HMR were higher in endotype 1 than in controls (p = 0.001 and p < 0.0001, respectively), suggesting structural microvascular remodeling. Conversely, endotype 2 was comparable to controls. A 13/32 (41%) patients in endotype 1 died in a follow up of 28 years and mortality rate was comparable to endotype 3 (14/31, 45%). However, CCFVR was < 80 cm/s in all 13 deaths of endotype 1 (characterized by preserved CFVR). At multivariable analysis, CMD, DPVh < 75 cm/s and CCFVR < 80 cm/s were independent predictors of mortality. The inclusion of CCFVR < 80 cm/s to models with clinical indicators of mortality better predicted survival, compared to only adding CMD or DPVh < 75 cm/s (p < 0.0001 and p = 0.03, respectively).ConclusionA normal CFVR could hide detection of microvasculopathy with high flow resistance and low flow velocities at rest. This microvasculopathy seems to be secondary to factors unrelated to HT (less rejections and more often diabetes). The combined use of CFVR and CCFVR provides more complete clinical and prognostic information on coronary microvasculopathy in HT.

Background: The aim of this study was to assess the role of cardiac and vascular parameters as all-cause mortality determinants in patients suffering from gynecological cancers. Methods: This was an observational, prospective, non-randomized, and non-controlled study. Forty-seven consecutive patients (mean age: 58 ± 13 years) were enrolled after cancer staging. All patients underwent evaluation of vascular (common carotid intima-media thickness (mean C-IMT), flow-mediated dilation of the brachial artery (FMD), and antero-posterior diameter of the infrarenal abdominal aorta (APAO)) and cardiac function and morphology before cancer-related interventions. A 6-year follow-up was carried out to assess the overall survival of the whole population. Results: Twenty patients (42%) died by the time of the 6-year follow-up. The brachial artery FMD values were higher in the survivors than the non-survivors (9.71 ± 3.53% vs. 6.13 ± 2.62%, p < 0.001), as well as the LVEF (60.8 ± 3.0% vs. 57.8 ± 4.4%, p = 0.009). There were no differences in the mean C-IMT, APAO, and other echocardiographic parameters. ROC curve analysis identified a baseline LVEF < 57% and FMD value < 5.8% as the best cut-offs. Kaplan–Meier evaluation showed that the LVEF, tricuspid annular plane systolic excursion, and FMD were the best predictors of all-cause mortality, although only the LVEF and FMD were confirmed in multivariate Cox regression analysis. Conclusions: The LVEF and brachial artery FMD are independent prognostic determinants in patients with gynecological cancers.

The introduction of high-sensitivity cardiac troponin allowed identifying a proportion of subjects with chest pain and electrocardiographic changes suggestive of myocardial infarction showing n = 15), MINOCA (n = 14) and TTS (n = 9) groups. The aim was to estimate the value of pFAI in these groups compared to 12 controls. To evaluate the coronary inflammation “time course,” 20 patients underwent CMR and coronary CT scan within 8 days from the onset, the others within 60 days. There were higher values of pFAI in myocarditis (−86.45 HU), MINOCA (−84.63 HU) and TTS (−84.79 HU) compared to controls (−96.02 HU; p = 0.0077). Among patients who underwent CT within 8 days from onset, the MINOCA had a significantly higher pFAI value (−76.91 HU) compared to the control group (−96.02 HU; p = 0.0001). In the group that underwent CT later than 8 days, elevated pFAI values persisted only in the myocarditis and TTS groups, and there was no difference between MINOCA and controls. Our study shows that in patients with a diagnosis of MINOCA, there is acute coronary inflammation, which is more evident within one week from the acute event but tends to disappear with time.

Background: The long-term efficacy of low-dose aspirin for primary prevention of cardiovascular (CV) events in postmenopausal women with type-2 diabetes is controversial. Therefore, it is recommended only on an individual basis, recommendation of grade C. Methods: We enrolled 275 consecutive postmenopausal women with type-2 diabetes, without an increased bleeding risk and without preexisting CV disease as coronary artery disease, stroke, and peripheral vascular disease, but with a high risk assessed by score >10%, aged 60–69 years. All were receiving aspirin (75–100 mg daily), aspirin group (AG). 170 postmenopausal women with type-2 diabetes and without preexisting cardiovascular (CV) disease, but not on aspirin treatment, despite a high risk assessed by score >10%, were control group (CG). Mean age was 66 ± 4 years for AG and 65 ± 7 years for CG. Our goal was to identify the prevalence of low-dose aspirin prescriptions in these populations according to different clinical conditions. Results: Women with only high risk were 41/275 (15%) on AG and 72/170 (42.3%) on CG, Chi-squared 41, Odds ratio 0.2, c.i. 95%, P < 0.0001. Women affected by metabolic syndrome were 105/275 (38.1%) on AG and 47/170 (27.6%) on CG, Chi-squared 5.1, Odds ratio 1.6, c.i. 95%, P < 0.02. Women affected by metabolic cardiomyopathy were 111/275 (40.3%) on AG and 44/170 (25.9%) on CG, Chi-squared 8, Odds ratio 1.8, c.i. 95%, P < 0.004. Women affected by diabetic cardiomyopathy were 18/275 (6.6%) on AG and 7/170 (4.2%) on CG, Chi-squared 1.2, Odds ratio 16, c.i. 95%, P < 0.2 n.s. Conclusions: Low-dose aspirin in our population is prescribed preferentially in postmenopausal women with type-2 diabetes when affected by metabolic syndrome or metabolic cardiomyopathy, at the opposite women with only high risk have lower chance to receive aspirin.

Pure autonomic failure is challenging as it can be the presenting feature of a central nervous system syncleinopathy such as Parkinson’s disease (PD) or multiple system atrophy (MSA). Because the prognosis of MSA and PD is so different, predictive features for a possible conversion can be extremely valuable. In this paper, we report three cases (two with autopsy-proven diagnosis) that had isolated AF for many years before converting to MSA or PD. Of all the tests that were performed during the premotor stage, Iodine-123-meta-iodobenzylguanidine (MIBG) myocardial scintigraphy was predictive of the conversion to MSA. We suggest that MIBG myocardial scintigraphy, when performed in patients with isolated AF, may be a valuable predictor of conversion to MSA. On the contrary, the role of such test in parkinsonian patients irrespective of the presence of AF is still to be clarified.