Search Results (28)

Background and Objectives: Nonischemic cardiomyopathies comprise a wide spectrum of heart muscle disorders characterized by different morphological, functional, and tissue abnormalities. Cardiovascular magnetic resonance (CMR) represents the gold standard imaging modality for assessing cardiac morphology, systolic function, and tissue characterization, thereby aiding in early diagnosis, precise phenotyping, and tailored treatment. The aim of this review is to provide an up-to-date overview of CMR techniques for studying myocardial perfusion and their applications to nonischemic cardiomyopathy, not only to rule out an underlying ischemic aetiology but also to investigate the pathophysiological characteristics of microcirculatory dysfunction in these patients. Materials and Methods: We performed a structured review of the literature focusing on first-pass gadolinium perfusion sequences, stress protocols, and emerging pixel-wise perfusion mapping approaches. Studies were selected to illustrate the methods for image acquisition, post-processing, and quantification of myocardial blood flow (MBF) and myocardial perfusion reserve (MPR), as well as to highlight associations with clinical endpoints. Results: First-pass CMR perfusion imaging reliably detects diffuse and regional microvascular dysfunction across cardiomyopathies. Semi-quantitative parameters (e.g., upslope, MPRI) and quantitative MBF mapping (mL/g/min) have demonstrated that impaired perfusion correlates with disease severity, extent of fibrosis, and adverse outcomes, including heart failure hospitalization, arrhythmias, and mortality. Novel automated pixel-wise mapping enhances reproducibility and diagnostic accuracy, distinguishing coronary microvascular dysfunction from balanced three-vessel disease. Microvascular dysfunction—present in approximately 50–60% of dilated cardiomyopathy (DCM), 40–80% of hypertrophic cardiomyopathy (HCM), and >95% of cardiac amyloidosis (CA) patients—has emerged as a key driver of adverse outcomes. Perfusion defects appear early, often preceding overt hypertrophy or fibrosis, and provide incremental prognostic value beyond conventional CMR metrics. Conclusions: CMR represents a powerful tool for detecting myocardial perfusion abnormalities in nonischemic cardiomyopathies, improving phenotyping, risk stratification, and personalized management. Further standardization of quantitative perfusion techniques will facilitate broader clinical adoption. Full article

Background: The stroke–heart syndrome refers to incident cardiac complications post stroke. This study aims to evaluate the stroke–heart syndrome by determining the rate and predictors of readmission for cardiac disease within 30 days of hospitalization for cerebral infarction. Methods: Data from the United States Nationwide Readmissions Database (2018 to 2020) were analyzed to identify rates and factors associated with 30-day readmissions for heart disease following cerebral infarction, excluding patients with atrial fibrillation, heart failure and myocardial infarction during admission with cerebral infarction. Results: There were 3,115,850 hospital admissions for cerebral infarction, and 75,440 admissions (2.4%) were readmitted with new onset cardiac events within 30 days of discharge. This included 36,310 (1.4%) readmissions for heart failure, 35,900 (1.1%) readmissions for atrial fibrillation, 17,465 (0.5%) readmissions for acute myocardial infarction, 810 (0.03%) readmissions for ventricular arrhythmias and 700 (0.02%) readmissions for Takotsubo syndrome. Readmitted patients were older (median age of 73 years vs. 68 years, p < 0.001) and had a longer length of stay for initial admission (median of 4 days vs. 3 days, p < 0.001). The most significant predictors of readmission were elective admission (OR 2.00, 95%CI 1.89–2.13, p < 0.001), cancer (OR 1.91, 95%CI 1.81–2.01, p < 0.001), chronic kidney disease (OR 1.80, 95%CI 1.73–1.87, p < 0.001), previous myocardial infarction (OR 1.59, 95%CI 1.50–1.69, p < 0.001) and liver failure (OR 1.34, 95%CI 1.06–1.68, p = 0.013). Palliative care was linked to a reduced odds of readmission (OR 0.36, 95%CI 0.31–0.41, p < 0.001). Conclusions: New cardiac-related hospital readmissions within 30 days after ischemic stroke occur in 2.4% of patients, with elective admission and cancer being a strong predictor of readmissions. Full article

Acute spinal cord injury (SCI) often results in severe neurologic deficits, with hemodynamic instability contributing to secondary ischemic damage. Beyond surgical decompression, maintaining adequate mean arterial pressure (MAP) is key to enhancing spinal cord perfusion and oxygenation. Vasopressor therapy is frequently used to achieve hemodynamic stability, but optimal MAP targets and vasopressor selection remain controversial. This review explores updated guidelines and current evidence regarding MAP management and the use of vasopressors in SCI, focusing on their impact on spinal cord perfusion and neurologic outcomes. Recent studies highlight the role of durotomy in directly improving spinal cord perfusion pressure (SCPP) by reducing intraspinal pressure (ISP), offering a complementary mechanical intervention as part of pharmacologic therapies. Recent guidelines suggest an MAP range of 75–80 mmHg as a lower limit and 90–95 mmHg as an upper limit for 3–7 days post-injury, highlighting the need for personalized hemodynamic management. Norepinephrine is commonly preferred due to its balanced effects on peripheral vascular resistance and spinal cord perfusion pressure (SCPP), though dopamine, phenylephrine, and dobutamine each offer unique hemodynamic profiles suited to specific clinical scenarios. Despite their benefits, vasopressors carry significant risks, including arrhythmias and potential myocardial strain, necessitating careful selection based on individual patient factors. Further research is needed to refine vasopressor use and establish evidence-based protocols that optimize neurologic recovery, alongside continued exploration of SCPP as a potential therapeutic target. Full article

Introduction. Post-coronavirus disease-2019 (COVID-19) patients may develop cardiac symptoms. We hypothesized that cardiovascular magnetic resonance (CMR) can assess the background of post-COVID-19 cardiac symptoms using multi-parametric evaluation. We aimed to conduct an investigation of symptomatic patients with post-COVID-19 syndrome using CMR (INSPIRE-CMR). Methods. INSIPRE-CMR is a retrospective multicenter study including 174 patients from five centers referred for CMR due to cardiac symptoms. CMR was performed using 3.0 T/1.5 T system (24%/76%, respectively). Myocardial inflammation was determined by the updated Lake Louise criteria. Results. Further, 174 patients with median age of 40 years (IQR: 26–54), 72 (41%) were women, and 17 (9.7%) had a history of autoimmune disease, muscular dystrophy, or cancer. In total, 149 (86%) patients were late gadolinium enhanced (LGE)-positive with a non-ischemic pattern, and of those evaluated with the updated Lake Louise criteria, 141/145 (97%) had ≥1 pathologic T1 index. Based on the T2-criterion, 62/173 (36%) patients had ≥1 pathologic T2 index. Collectively, 48/145 (33%) patients had both positive T1- and T2-criterion. A positive T2-criterion or a combination of a positive T1- and T2-criterion were significantly more common amongst patients with severe COVID-19 [45 (31%) vs. 17 (65%), p = 0.001 and 32 (27%) vs. 16 (64%), p < 0.001, respectively]. During the one-year evaluation, available for 65/174 patients, shortness of breath, chest pain, and arrhythmia were identified in 7 (4%), 15 (8.6%), and 43 (24.7%), respectively. CMR evaluation, available in a minority of them, showed mildly reduced LVEF, while nat T1 mapping and EVC remained at levels higher than the normal values of the local MRI units. Conclusions. The majority of post-COVID-19 patients with cardiac symptoms presented non-ischemic LGE and abnormalities in T1 and T2-based indices. Multi-parametric CMR reveals important information on post-COVID-19 patients, supporting its role in short/long-term evaluation. Full article

Background and Objectives: This study explored the effect of paired remote ischemic preconditioning (RIPC), involving both recipients and living donors, on cardiovascular stress in recipients after living-donor kidney transplantation (LDKT). The analysis included an assessment of the impact on cardiovascular biomarkers and post-transplant cardiovascular clinical events. Materials and Methods: A retrospective observational cohort study of 520 adult LDKT patients was conducted, employing propensity score matching (PSM) to analyze perioperative factors. The patients were allocated to no-RIPC (n = 260) and paired-RIPC (n = 260) groups. The two groups were compared with respect to high-sensitivity troponin I (hsTnI) and B-type natriuretic peptide (BNP) levels, corrected QT (QTc) intervals, the occurrence of arrhythmia, and the requirement for cardiovascular interventions. Results: After PSM, there were no significant differences in perioperative parameters between the no-RIPC and paired-RIPC groups. However, on postoperative day (POD) 1, higher hsTnI levels and QTc interval prolongation, as well as higher incidences of arrhythmia and the need for percutaneous coronary intervention (PCI), were determined in the no-RIPC group than in the paired-RIPC group. The associations between paired RIPC and improved cardiovascular outcomes were significant, including reduced odds of elevated hsTnI levels, QTc prolongation, and arrhythmia. The no-RIPC group also had longer intensive care unit (ICU) stays, and higher rates of rescue dialysis. Conclusions: Paired-RIPC involving recipients and donors effectively reduces cardiovascular stress markers and improves postoperative cardiovascular outcomes in LDKT recipients, underscoring its potential as a protective strategy against perioperative cardiovascular risks. Full article

Stroke–heart syndrome (SHS), a critical yet underrecognized condition, encompasses a range of cardiac complications that arise following an ischemic stroke. This narrative review explores the pathophysiology, clinical manifestations, and implications of SHS, focusing on the complex interplay between the brain and the heart. Acute ischemic stroke (AIS) triggers autonomic dysfunction, leading to a surge in catecholamines and subsequent myocardial injury. Our review highlights the five cardinal manifestations of SHS: elevated cardiac troponin (cTn) levels, acute myocardial infarction, left ventricular dysfunction, arrhythmias, and sudden cardiac death. Despite the significant impact of these complications on patient outcomes, there is a notable absence of specific guidelines for their management. Through a comprehensive literature search, we synthesized findings from recent studies to elucidate the mechanisms underlying SHS and identified gaps in the current understanding. Our findings underscore the importance of early detection and multidisciplinary management of cardiac complications post-stroke. Future research should focus on establishing evidence-based protocols to improve clinical outcomes for stroke patients with SHS. Addressing this unmet need will enhance the care of stroke survivors and reduce mortality rates associated with cardiac complications. Full article

Background/Objectives: Atrial fibrillation (AF) and flutter (AFL) are the most common cardiac arrhythmias worldwide. Cardiovascular complications are a common manifestation of acute and post-acute COVID-19 infection. We aimed to analyze the nationwide trends in clinical characteristics and outcomes of patients hospitalized for AF/AFL before and during the COVID-19 outbreak in the U.S. Methods: This study is a retrospective analysis of patients, aged 18 and older, hospitalized for AF/AFL in the U.S. between 2016 and 2020. We drew data from the National Inpatient Sample (NIS) database. Baseline sociodemographic and clinical data, as well as outcomes including stroke, acute coronary syndrome (ACS), and mortality, were analyzed. Multivariable analysis was performed to identify independent associations between the different clinical and demographic characteristics and the composite endpoint of Mortality/ACS/Stroke. Results: An estimated total of 2,163,699 hospitalizations for AF/AFL were identified. The hospitalization volume between 2016 and 2019 was stable, averaging 465,176 a year, followed by a significant drop to 302,995 in 2020. Patients’ median age was 72 years (IQR 62–80), 50.9% were male, and 81.5% were white. The composite endpoint steadily increased from 6.5% in 2016 to 11.8% in 2020 (P_trend < 0.001). In a multivariable regression analysis, age > 75 (OR: 1.35; 95% CI 1.304–1.399, p < 0.001), ischemic heart disease (OR: 1.466; 95% CI: 1.451–1.481; p < 0.001), and chronic kidney disease (OR: 1.635; 95% CI: 1.616–1.653; p < 0.001) were associated with the composite endpoint. COVID-19 was associated with the composite endpoint outcome in the year 2020 (OR: 1.147; 95% CI: 1.037–1.265; p = 0.007). Conclusions: Hospitalization for AF/AFL dropped significantly during the first year of the COVID-19 pandemic outbreak, possibly due to patients’ avoidance of hospital visits. The composite endpoint of Mortality/ACS/Stroke uptrended significantly during the study period. COVID-19 was shown to be independently associated with the adverse composite outcome Mortality/ACS/Stroke. Full article

Background: Donor shortage limits the utilization of heart transplantation, making it available for only a fraction of the patients on the transplant waiting list. Therefore, continuous-flow left ventricular assist devices (CF-LVADs) have evolved as a standard of care for end-stage heart failure. It is imperative therefore to investigate long-term survival in this population. Methods: This study assesses the impact of demographics, infections, comorbidities, types of cardiomyopathies, arrhythmias, and end-organ dysfunction on the long-term survival of LVAD recipients. The TriNetX database comprises de-identified patient information across healthcare organizations. The log-rank test assessed post-implant survival effects, while Cox regression was used in the univariate analysis to obtain the Hazard Ratio (HR). All analyses were conducted using the Python programming language and the lifelines library. Results: This study identified CMV, hepatitis A exposure, atrial fibrillation, paroxysmal ventricular tachycardia, ischemic cardiomyopathy, renal dysfunction, diabetes, COPD, mitral valve disease, and essential hypertension as risk factors that impact long-term survival. Interestingly, hypokalemia seems to have a protective effect and gender does not affect survival significantly. Conclusions: This is the first report of a detailed long-term survival assessment of the LVAD population using a decoded database. Full article

Introduction: Post-transplant cardiovascular disease (PTCVD) poses a significant challenge in kidney transplantation, potentially impacting graft outcomes and patient survival. This retrospective study aimed to investigate the incidence, risk factors, and consequential impact of PTCVD in kidney transplant recipients (KTRs) devoid of pre-existing cardiovascular disease (CVD). Method: The cohort comprised 1114 KTRs, with 749 individuals included after excluding those with pre-existing CVD and early graft loss. PTCVD encompasses ischemic heart disease, myocardial infarction, arrhythmias, heart failure, stroke, peripheral vascular disease, and valvular heart disease. Competing risk regression analysis was performed to identify predictors of PTCVD, while Cox proportional hazards analysis assessed the impact of PTCVD on graft and recipient survival. Results: The cumulative incidence of PTCVD at 5, 10, and 20 years was 5.4%, 14.3%, and 22.5%, respectively. Competing risk regression identified increased age (sub-hazard ratio [SHR], 1.22; p = 0.036) per decade, duration of dialysis (SHR, 1.07; p = 0.048) per year on dialysis, and the slope of the estimated glomerular filtration rate (SHR, 1.08; p = 0.008) mL/min/year decline as independent predictors of higher-risk PTCVD. A higher baseline estimated glomerular filtration rate (eGFR) was protective (SHR, 0.98; p = 0.032). PTCVD was not significantly associated with death-censored graft loss (adjusted hazard ratio [aHR] 1.31; p = 0.48) but was correlated with higher all-cause graft loss (aHR, 1.71; p = 0.011) and recipient mortality (aHR, 1.97; p = 0.004). Conclusion: This study provides insights into PTCVD predictors. Although not directly associated with graft loss, PTCVD significantly correlates with heightened mortality in kidney transplant recipients, emphasizing the need for enhanced clinical management and surveillance strategies. Full article

COVID-19 is primarily a respiratory disease, but numerous studies have indicated the involvement of various organ systems during the course of illness. We conducted a comprehensive review of atypical complications of COVID-19 with their incidence range (IR) and their impact on hospitalization and mortality rates. We identified 97 studies, including 55 research articles and 42 case studies. We reviewed four major body organ systems for various types of atypical complications: (i) Gastro-intestinal (GI) and hepatobiliary system, e.g., bowel ischemia/infarction (IR: 1.49–83.87%), GI bleeding/hemorrhage (IR: 0.47–10.6%), hepatic ischemia (IR: 1.0–7.4%); (ii) Neurological system, e.g., acute ischemic stroke/cerebral venous sinus thrombosis/cerebral hemorrhage (IR: 0.5–90.9%), anosmia (IR: 4.9–79.6%), dysgeusia (IR: 2.8–83.38%), encephalopathy/encephalitis with or without fever and hypoxia (IR: 0.19–35.2%); (iii) Renal system, e.g., acute kidney injury (AKI)/acute renal failure (IR: 0.5–68.8%); (iv) Cardiovascular system, e.g., acute cardiac injury/non-coronary myocardial injury (IR: 7.2–55.56%), arrhythmia/ventricular tachycardia/ventricular fibrillation (IR: 5.9–16.7%), and coagulopathy/venous thromboembolism (IR: 19–34.4%). This review encourages and informs healthcare practitioners to keenly monitor COVID-19 survivors for these atypical complications in all major organ systems and not only treat the respiratory symptoms of patients. Post-COVID effects should be monitored, and follow-up of patients should be performed on a regular basis to check for long-term complications. Full article

The scar border zone is a main source of reentry responsible for ischemic ventricular tachycardia (VT). We evaluated the effects of mesenchymal stem cell (MSC) injection into the scar border zone on arrhythmic risks in a post-myocardial infarction (MI) animal model. Rabbit MI models were generated by left descending coronary artery ligation. Surviving rabbits after 4 weeks underwent left thoracotomy and autologous MSCs or phosphate-buffered saline (PBS) was administered to scar border zones in two rabbits in each group. Another rabbit without MI underwent a sham procedure (control). An implantable loop recorder (ILR) was implanted in the left chest wall in all animals. Four weeks after cell injections, ventricular fibrillation was induced in 1/2 rabbit in the PBS group by electrophysiologic study, and no ventricular arrhythmia was induced in the MSC group or control. Spontaneous VT was not detected during ILR analysis in any animal for 4 weeks. Histologic examination showed restoration of connexin 43 (Cx43) expression in the MSC group, which was higher than in the PBS group and comparable to the control. In conclusion, MSC injections into the MI scar border zone did not increase the risk of VT and were associated with favorable Cx43 expression and arrangement. Full article

Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43³⁶⁸). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43³⁶⁸ levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level. Full article

Aims: Patients after heart transplantation (HTX) often require oral anticoagulants (OACs) due to atrial arrhythmias or thromboembolic events but little is known about the post-transplant use of direct oral anticoagulants (DOACs). We investigated the frequency, indications, and complications of DOACs and vitamin K antagonists (VKAs) after HTX. Methods: We screened all adult patients for the use of post-transplant OACs who underwent HTX at Heidelberg Heart Center between 2000 and 2021. Patients were stratified by type of OAC (DOAC or VKA) and by DOAC agents (apixaban, dabigatran, edoxaban, or rivaroxaban). Indications for OACs comprised atrial fibrillation, atrial flutter, pulmonary embolism, upper and lower extremity deep vein thrombosis, as well as intracardiac thrombus. Results: A total of 115 of 459 HTX recipients (25.1%) required OACs, including 60 patients with DOACs (52.2%) and 55 patients with VKAs (47.8%). Concerning DOACs, 28 patients were treated with rivaroxaban (46.7%), 27 patients with apixaban (45.0%), and 5 patients with edoxaban (8.3%). We found no significant differences between both groups concerning demographics, immunosuppressive drugs, concomitant medications, indications for OACs, ischemic stroke, thromboembolic events, or OAC-related death. Patients with DOACs after HTX had a significantly lower one-year rate of overall bleeding complications (p = 0.002) and a significantly lower one-year rate of gastrointestinal hemorrhage (p = 0.011) compared to patients with VKAs after HTX in the Kaplan–Meier estimator. Conclusions: DOACs were comparable to VKAs concerning the risk of ischemic stroke, thromboembolic events, or OAC-related death but were associated with significantly fewer bleeding complications in HTX recipients. Full article

Background: Checkpoint inhibitors, such as PD-1 inhibitors (nivolumab, pembrolizumab) and anti-CTLA-4 (CD152) (ipilimumab), are widely used in metastatic melanoma, and most immune-related adverse events are known. Several cardiovascular AEs (CVAEs) associated with immune checkpoint inhibitor exposure have been reported in post-marketing surveillance studies and represent major issues for patients with melanoma during and after cancer treatment. Data on CVAES induced by immune checkpoint inhibitors in melanoma, especially incidence and risk factors, are lacking. Methods: A systematic review of the literature up to 31 August 2020 was performed in Medline, the Cochrane Central Register of Controlled Trials (CENTRAL), and the ClinicalTrials.gov register according to prespecified selection criteria from inception to 7 April 2020. Statistics were performed on 3289 patients from five randomized clinical trials on melanoma. Results: Patients with melanoma treated with immune checkpoint inhibitors had a significant risk of presenting dyslipidemia (Peto OR: 4.74, 95% CI: 2.16–10.41, p < 0.01, I2 = 0%, p = 0.94). The Peto OR was numerically significant for pericarditis, myocarditis, heart failure, myocardial infarction, cerebral ischemia, high pulmonary pressure, blood high pressure, arrhythmias, endocarditis, and conduction disturbances, but the confidence interval was not significant. The risk of CVAEs was not statistically different between melanoma treated with immune checkpoint inhibitors and other tumors treated with immune checkpoint inhibitors (range of p-value from 0.13 to 0.95). No interaction between follow-up length and CVAE reporting was found. Conclusions: Our study underlines that checkpoint inhibitors used for melanoma increase CVAEs, especially dyslipidemia, which could pave the way to chronic inflammatory processes, atherosclerosis, and, finally, ischemic cardiopathy. These cardiovascular adverse events could be acute or delayed, justifying the monitoring of lipidic biology and a baseline cardiology consultation. Full article

Background: Leptin is an obesity-associated adipokine that has been implicated in cardiac protection against ischemia-reperfusion injury (IRI). In this study, concentration-dependent effects of leptin on myocardial IRI were investigated in the isolated rat heart. In addition, we analyzed myocardial miRNAs expression in order to investigate their potential involvement in leptin-mediated cardioprotection. Methods: The effect of leptin on IRI was examined in Langendorff-perfused rat hearts preconditioned with two leptin concentrations (1.0 nM and 3.1 nM) for 60 min. The hearts were subjected to 30 min global ischemia and 120 min reperfusion with buffer containing leptin in the respective concentration. Heart function and arrhythmia incidence were analyzed. Infarct size was assessed histochemically. Expression of miRNA-144, -208a, -378, and -499 was analyzed in the ventricular myocardium using RT-PCR. Results: The addition of 1.0 nM leptin to the buffer exerted an infarct-limiting effect, preserved post-ischemic ventricular function, and prevented reperfusion arrhythmia compared to 3.1 nM leptin. Myocardial expression of miRNA-208a was decreased after heart exposure to 1.0 nM leptin and significantly elevated in the hearts perfused with leptin at 3.1 nM. Conclusion: Acute administration of leptin at low dose (1.0 nM) results in cardiac protection against IRI. This effect is associated with reduced myocardial expression of miRNA-208a. Full article