There exist two opposing perspectives regarding reactive oxygen species (ROS) and their roles in angiogenesis and cardiovascular system, one that favors harmful and causal effects of ROS, while the other supports beneficial effects. Recent studies have shown that interaction between ROS in different sub-cellular compartments plays a crucial role in determining the outcomes (beneficial vs. deleterious) of ROS exposures on the vascular system. Oxidant radicals in one cellular organelle can affect the ROS content and function in other sub-cellular compartments in endothelial cells (ECs). In this review, we will focus on a critical fact that the effects or the final phenotypic outcome of ROS exposure to EC are tissue- or organ-specific, and depend on the spatial (subcellular localization) and temporal (duration of ROS exposure) modulation of ROS levels.

Cardiovascular diseases (CVD) are one of the prime causes of mortality worldwide. Experimental animal models have become a valuable tool to investigate and further advance our knowledge on etiology, pathophysiology and intervention. They also provide a great opportunity to understand the contribution of different genes and effector molecules in the pathogenesis and development of diseases at the sub-cellular levels. High levels of reactive oxygen species (ROS) have been associated with the progression of CVD such as ischemic heart disease (IHD), myocardial infarction, hypertension, atherosclerosis, aortic aneurysm, aortic dissection and others. On the contrary, low levels of antioxidants were associated with exacerbated cardiovascular event. Major focus of this review is on vascular pathogenesis that leads to CVD, with special emphasis on the roles of oxidant/antioxidant enzymes in health and disease progression in vascular cells including vascular endothelium. The major oxidant enzymes that have been implicated with the progression of CVD include NADPH Oxidase, nitric oxide synthase, monoamine oxidase, and xanthine oxidoreductase. The major antioxidant enzymes that have been attributed to normalizing the levels of oxidative stress include superoxide dismutases, catalase and glutathione peroxidases (GPx), and thioredoxin. Cardiovascular phenotypes of major oxidants and antioxidants knockout and transgenic animal models are discussed here.

Takotsubo cardiomyopathy is described as transient, ventricular dysfunction. A relatively rare pathology accounting for 0.02% of hospitalizations, recurrent episodes are even less common, occurring at 1-6%. Here, we present a case of an elderly woman presenting with multiple, recurrent episodes of takotsubo cardiomyopathy. Similarities and differences between our case and others presented in literature are compared. Our case highlights the importance of maintaining a broad differential when presented with multiple episodes of recurrent, acute heart failure in the setting of chest pain and ST segment elevations. Keywords: Takotsubo cardiomyopathy; Acute coronary syndrome; ST elevation; heart failure; apical myocardial ballooning

BACKGROUND:Lyme carditis typically presents with atrio-ventricular block; however, other cardiac manifestations, including varying EKG changes, myopericarditis and new-onset heart failure, can occur. CASE REPORT:We report a case of a 52-year-old woman with past medical history significant for hypertension, chronic obstructive pulmonary disease, and chronic back pain who presented with new-onset heart failure in the setting of Lyme carditis. She presented with exertional dyspnea requiring supplemental oxygen, subjective fever, chills, fatigue, and arthralgia of 2-week duration. Her vital signs were consistent with hypotension and persistent bradycardia. An EKG displayed T-wave flattening in the anterior pre-cordial leads. Further work-up was suggestive of bilateral pulmonary edema and interstitial infiltrates, which required antibiotics and diuretics. Echocardiography demonstrated new-onset mildly depressed LV systolic dysfunction. Interestingly, coronary CTA revealed coronary arteries with no evidence of stenosis or plaque. She was found to have positive Lyme IgM and lgG antibodies. A diagnosis of Lyme myocarditis was considered and her antibiotic course was extended following multidisciplinary consensus. CONCLUSIONS:This case report seeks to create awareness of the varying and atypical presentations of Lyme carditis, including new-onset heart failure in a patient without prior history of ischemic heart disease and uncommon EKG changes.

We present a rare case of CardioMEMS device migration six years post-implantation. Much is still being learned about endothelization of pulmonary vasculature and this case highlights the importance of device surveillance and device-related complications.

Next-generation Bruton’s tyrosine kinase inhibitors (BTKis) such as acalabrutinib and zanubrutinib have improved treatment outcomes in B-cell malignancies, including chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL), and Waldenström macroglobulinemia (WM), while reducing off-target toxicities compared to ibrutinib. However, their comparative cardiovascular safety profiles remain poorly characterized. This study evaluates real-world cardiovascular and clinical outcomes between zanubrutinib and acalabrutinib using a large multi-center database. We conducted a retrospective cohort study using the TriNetX Research Network (October 2017–December 2024) including adult patients with CLL, MCL, WM, or small B-cell lymphoma treated with zanubrutinib or acalabrutinib. Patients with prior exposure to other BTKis were excluded. After 1:1 propensity score matching, 2887 patients were included in each cohort. We assessed one-year outcomes including new-onset atrial fibrillation/flutter, cerebral infarction, hypertension, and all-cause mortality using Cox proportional hazards modeling. The rate of AF/flutter events observed in the zanubrutinib group (4.05%) was numerically lower compared to the acalabrutinib group (5.25%). Time-to-event analysis did not demonstrate a statistically significant difference in AF risk over time (HR 0.777, 95% CI 0.597–1.012; p = 0.06), which was similar in binary analysis (OR 0.761, 95% CI 0.581–0.997; p = 0.05). Cerebral infarction rates were similar between groups (1.09% vs. 1.12%), with no significant difference in time-to-event analysis (HR 0.984, 95% CI 0.596–1.626; p = 0.95) or binary analysis (p = 0.91). There was no significant difference in onset of hypertension in the zanubrutinib cohort (HR 1.199, 95% CI 0.957–1.501; p = 0.11) All-cause mortality was not statistically significant between the two groups (HR 0.865, 95% CI 0.740–1.012; p = 0.07). In this large, real-world analysis, fewer AF/flutter events were observed with zanubrutinib at one year; however, time-to-event analysis did not demonstrate a statistically significant difference in AF risk over time. Notably, hypertension, cerebral infarction, and all-cause mortality occurred at similar rates. This suggests zanubrutinib and acalabrutinib share similar cardiovascular safety profiles overall. However these findings are hypothesis-generating and require prospective validation before definitive conclusions about cardiovascular risk can be drawn.