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Background Heroin use may work synergistically with human immunodeficiency virus (HIV) infection to cause greater immune dysregulation than either factor alone. Unraveling how this affects end-organ disease is key as it may play a role in the excess mortality seen in people with HIV (PWH) who use heroin despite access to care and antiretroviral therapy. Methods This is a prospectively enrolled, cross-sectional study of adults with and without HIV who use and do not use heroin using (18)F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) to compare tissue-specific inflammation including aortic (target-to-background ratio [TBR]), splenic, and bone marrow (standardized uptake value [SUV]). Results A total of 120 participants were enrolled. The unadjusted mean difference in aortic TBR was 0.43 between HIV-positive [HIV+] heroin+ and HIV+ heroin-negative [heroin−] (P = .02); however, among HIV−, aortic TBR was similar regardless of heroin-use status. Further, HIV-by-heroin-use status interaction was significant (P = .02), indicating that the relationship between heroin use and higher aortic TBR depended on HIV status. On the other hand, both HIV (1.54 vs 1.68; P = .04, unadjusted estimated means for HIV+ vs HIV−) and heroin use were associated with lower bone marrow SUV, although the effect of heroin depended on sex (heroin-use-by-sex interaction, P = .03). HIV-by-heroin-use interaction was not significant for splenic or bone marrow SUV. Conclusions Aortic inflammation was greatest in PWH who use heroin, but paradoxically, bone marrow activity was the least in this group, suggesting complex and possibly divergent pathophysiology within these different end organs.

Chronic systemic inflammation is associated with an increased risk of heart failure (HF). We sought to determine the association between biomarkers of systemic inflammation interleukin (IL)-6, IL-2, tumor necrosis factor alpha (TNF-α), and C-reactive protein (CRP) with those of HF and its subtypes. We hypothesize that inflammatory biomarkers IL-6, IL-2, TNF-α, and CRP are associated with HF and its subtypes. We included participants from the Multi-Ethnic Study of Atherosclerosis (a prospective population-based cohort study [2000 to 2002]), without a history of HF, and with available baseline inflammatory biomarkers. We explored the association of IL-6, IL-2, TNF-α, and CRP with incident HF, HF with reduced ejection fraction (left ventricular ejection fraction [LVEF]40%, HFrEF), HF with midrange EF (LVEF 40% to 50%, HFmrEF), and HF with preserved ejection fraction (LVEF50%, HFpEF). Among 6,814 participants, 195 developed HF over 10.9 years (56 HFrEF, 30 HFmrEF, and 57 HFpEF). In the models adjusted for clinical risk factors of HF, IL-6 (hazard ratio [HR] 1.33 per doubling; 95% confidence interval [CI] 1.10 to 1.60), TNF-α (HR 2.49 per doubling; 95% CI 1.18 to 5.28), and CRP (HR 1.18 per doubling; 95% CI 1.06 to 1.30) were associated with all HF, and IL-6 (HR 1.51 per doubling; 95% CI 1.09 to 2.10) and CRP (HR 1.21 per doubling; 95% CI: 1.01 to 1.45) were associated with incident HFpEF, whereas none of the examined biomarkers were associated with HFmrEF or HFrEF. In conclusion, inflammatory biomarkers (IL-6, TNF-α, and CRP) are independently associated with incident HF. IL-6 and CRP are associated with incident HFpEF but not HFrEF or HFmrEF. These findings suggest that activation of the IL-6/CRP pathway (as cause, consequence, or epiphenomenon) may be unique to HFpEF.

Acute myelogenous leukemia (AML) is one of the most common leukemias experienced in adults and conveys significant morbidity and mortality. While the traditional anthracycline based treatments of AML involves cytarabine, developments in alternatives (liposomal cytarabine, fludarabine, cladribine, azacitidine, decitabine), and targeted agents (midostaurin, gilteritinib, enasidenib, ivosidenib, gemtuzumab ozogamicin, and venetoclax) exist. Multiple cardiovascular adverse events, notably pericardial toxicity, have been observed in small studies; however, to date little is known about the comparative pericardial toxicity among these newer regimens. Due to the paucity of data, we sought to investigate the reported pericardial events and mortality associated with treatments for AML. Utilizing the Food and Drug Administration (FDA) Adverse Events Reporting System (FAERS), we identified all adverse events associated with FDA approved treatments for AML (2002-2022). Pericardial events were defined as pericarditis, pericardial effusion and tamponade. We excluded any individuals with age18 years old. Logistic regression was utilized to identify factors associated with pericardial events. Out of 94,262 reported adverse events, 675 pericardial toxicities were included (243 pericarditis, 479 tamponade). Pericardial events occurred less often in Cladribine (0.3%, P0.001), fludarabine (0.4%, P0.001), Venetoclax (0.3%, P0.001), enasidenib (0.3%, P value0.001), and ivosidenib (0.3%, P0.001) compared to Cytarabine (0.9%). Tamponade events occurred significantly less often in cladribine (0.1%, P0.001), fludarabine (0.4%, P = 0.001), enasidenib (0.1%, P = 0.006), ivosidenib (0.1%, P = 0.01), and venetoclax (0.1%, P0.001) compared to cytarabine 0.7%. After adjusting for age and sex, Cladribine (reporting odds ratio [ROR] 0.35 [95% CI 0.18-0.68], P = 0.008) and Fludarabine (ROR 0.65 [0.45-0.92], P = 0.03), venetoclax (ROR 0.57 [0.41-0.79], P0.001) remained significantly associated with lower incidence of reported pericardial events. While cytarabine has been the routinely used and/or drug of choice for induction chemotherapy for AML, alternatives like cladribine may have a greater safety profile regarding pericardial toxicities. Future studies should be directed at further investigating cardiovascular safety profiles of AML induction therapy.

Aneurysms complicated by rupture of the coronary arteries are exceedingly rare. Literature regarding management of mycotic aneurysms resulting in rupture is limited. Therefore, we describe a fascinating diagnosis, imaging progression and management of a ruptured mycotic coronary artery aneurysm.

When pericardial fluid accumulates and exceed the reserve volume of the pericardium or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may ensue, namely, cardiac tamponade (CT), characterised by the accumulation of pericardial fluid under pressure; constrictive pericarditis (CP), the result of scarring and loss of the normal elasticity of the pericardial sac; and effusive–constrictive pericarditis (ECP), characterised by the concurrence of a tense pericardial effusion and constriction of the heart by the visceral pericardium. Although relatively uncommon, prevalence estimates vary widely and depend on the nature of the cohorts studied, the methods used to diagnose ECP and the manner in which ECP is defined. Most cases of ECP are idiopathic, reflecting the frequency of idiopathic pericardial disease in general, and other causes include radiation, malignancy, chemotherapy, infection and postsurgical/iatrogenic pericardial disease. The diagnosis of ECP often becomes apparent when pericardiocentesis fails to decrease the right atrial pressure by 50% or to a level below 10 mm Hg. Important non-invasive diagnostic modalities include echocardiography, cardiac magnetic resonance and, to a lesser extent, cardiac CT. In cases with clear evidence of pericardial inflammation, a trial of an anti-inflammatory regimen is warranted. A complete pericardiectomy should be reserved for refractory symptoms or clinical evidence of chronic CP.

To investigate the patterns and demographic features of cardiovascular disease (CVD) death and subtypes myocardial infarction (MI), stroke, and heart failure in the pre-COVID-19 era (2018-2019) vs during the COVID-19 pandemic (2020-2021) in the United States.In this cross-sectional study, we used the US Multiple Cause of Death files for 2018 to 2021 to examine the trend of excess cause-specific deaths using International Classification of Diseases, Tenth Revision codes for CVD (I00 to I99), MI (I21 and I22), stroke (I60 to I69), and heart failure (I42 and I50). Our primary outcome was excess mortality from CVD and its 3 subtypes (MI, stroke, and heart failure) between prepandemic (2018-2019) and pandemic (2020-2021) years. We performed a subgroup analysis on race and month-to-month and year-to-year variation using χOverall, 3,598,352 CVD deaths were analyzed during the study period. There was a 6.7% excess CVD mortality, 2.5% MI mortality, and 8.5% stroke mortality during the COVID-19 pandemic (2020-2021) compared with the prepandemic era (2018-2019). Black individuals had higher excess CVD mortality (13.8%) than White individuals (5.1%; P.001). This remained consistent across subtypes of CVD, including MI (9.6% vs 1.0%; P.001), stroke (14.5% vs 6.9%; P.001), and heart failure (5.1% vs -1.2%; P.001).There has been a significant rise in CVD and subtype-specific mortality during the COVID-19 pandemic that has been persistent despite 2 years since the onset of the pandemic. Excess CVD mortality has disproportionately affected Black compared with White individuals. Further studies targeting and eliminating health care disparities are necessary.

Background The global pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused significant morbidity and mortality, not only through devastating lung injury, but also due to multiple malfunctions in the cardiovascular system. The primary aetiology is believed to be mediated through lung alveolar injury; however, a few published reports have linked SARS-CoV-2 to significant organ dysfunction, venous thrombo-embolism, and coagulopathy. In view of the fact that the utility of tissue plasminogen activator in this population is not well studied, we present this case of rapid improvement in oxygenation after successful lytic therapy for thrombus in transit in this patient with SARS-CoV-2. Case summary We discuss a patient admitted with SARS-CoV-2 pneumonia. Due to the development of dramatic hypoxia, he underwent echocardiography which demonstrated extensive thrombus in transit. He received successful thrombolytic therapy with tissue plasminogen activator, with subsequent improvement in oxygenation. The patient was successfully discharged home on 2 L of oxygen via nasal cannula, and continues to improve at follow-up with his cardiologist and primary care physician. Conclusion This case not only highlights embolic causes of hypoxia in SARS-CoV-2, but demonstrates the important utility of an echocardiogram and tissue plasminogen activator in this population.

Patients with chronic kidney disease (CKD) are at increased risk for peripheral arterial disease (PAD). A novel biomarker to accurately and reliably predict new onset PAD in high risk patients is needed. High sensitivity troponin (HsTP) is a new assay which allows detection of very low troponin levels with high precision. We sought to explore the association between HsTP and risk of PAD in CKD. The Chronic Renal Insufficiency Cohort (CRIC) is a prospective cohort of 3,939 individuals with mild to moderate CKD using age related criteria for glomerular filtration rate. High sensitivity troponin T was measured at study enrollment. Patients with previous history of PAD or coronary artery disease were excluded. Patients were followed for new-onset adjudicated PAD, and the association between HsTP and incident PAD was examined. A total of 2,909 participants free of PAD and coronary artery disease at enrollment were included in this analysis. Over a mean follow up 7.4 years [interquartile ranges 5.8 to 8.5] years, 79 (2.7%) patients developed PAD. The 3-, 6-, and 9-year incidence of PAD was 1.00%, 2.03%, and 2.72%, respectively. At 9 years, the cumulative rates of PAD increased with HsTP (Quartile 1: 0.3%, Quartile 2: 2.4%, Quartile 3: 3.7%, Quartile 4: 10.7%; p 0.001). After adjusting for clinical risk factors of PAD, patients in the third quartile (Hazards ratio 5.89, 95% confidence interval: 1.31 to 26.47, p = 0.021) and fourth quartile of HsTP (Hazards ratio 10.24, 95% confidence interval 2.23 to 47.08, p = 0.003) had higher risk of PAD compared with lowest quartile of HsTP. HsTP had good discrimination of PAD at 3 years (area under the curve [AUC] 0.76), 6 years (AUC 0.79) and 9 years (AUC 0.80). Addition of HsTP to Framingham risk score improved model discrimination of PAD. In conclusion, in patients with mild-moderate CKD, HsTP levels are associated with and predictive of risk of incident PAD. This association remains significant despite adjustment for traditional PAD risk factors and chronic kidney disease.

BACKGROUND: Patients with chronic kidney disease (CKD) are at increased risk for atrial fibrillation (AF). There is a need for novel biomarkers to reliably and accurately predict AF in this population. High sensitivity troponin (HsTP) allows detection of very low troponin concentrations. The utility of HsTP for evaluating the risk of AF in CKD has not been established. OBJECTIVE: We sought to explore the association between HsTP and the risk of incident AF in chronic kidney disease. METHODS: The Chronic Renal Insufficiency Cohort (CRIC) is a prospective cohort of 3939 individuals with mild to moderate CKD. HsTP was measured at study enrollment. Patients with prior history of AF were excluded. Patients were followed for new-onset AF, and the association between HsTP and incident AF was examined using Cox regression model. RESULTS: A total of 3,217 participants were included. Over a median follow up of 7.1 [IQR 5.0–8.4] years, 252 patients developed new-onset AF (12 events per 1000 person-year of follow-up). The incidence of new onset AF was 2.46%, 7.06%, and 11.5% at 3, 6 and 9 years, respectively. Compared with lowest quartile of HsTP (Q1), patients in third quartile of HsTP (HR 2.40, 95% CI: 1.58–3.65, P

While the classical apical ballooning takotsubo cardiomyopathy (TC) was first reported in the 1990s, the rarer mid-ventricular and basal variants were not formally recognized until recently and they remain poorly understood. In this case report, we describe a 67-year-old woman who, during her hospitalization for a subarachnoid hemorrhage and subsequent readmission, experienced multiple complications, each of which resulted in a different variant of TC. To our knowledge, this is the first report of a single patient developing all three variants of TC.

Cardiac allograft vasculopathy (CAV) is the leading cause of long-term graft dysfunction in patients with heart transplantation and is linked with significant morbidity and mortality. Currently, the gold standard for diagnosing CAV is coronary imaging with intravascular ultrasound during traditional invasive coronary angiography. Invasive imaging, however, carries increased procedural risk and expense to patients in addition to requiring an experienced interventionalist. With the improvements in non-invasive cardiac imaging modalities such as transthoracic echocardiography, computed tomography, magnetic resonance imaging and positron emission tomography, an alternative non-invasive imaging approach for the early detection of CAV may be feasible. In this systematic review, we explored the literature to investigate the utility of non-invasive imaging in diagnosis of CAV in3000 patients across 49 studies. We also discuss the strengths and weaknesses for each imaging modality. Overall, all 4 imaging modalities show good to excellent accuracy for identifying CAV with significant variations across studies. Majority of the studies compared non-invasive imaging with invasive coronary angiography without intravascular imaging. In summary, non-invasive imaging modalities offer an alternative approach to invasive coronary imaging for CAV. Future studies should investigate longitudinal non-invasive protocols in low-risk patients after heart transplantation.

People with HIV (PWH) experience increased systemic inflammation and monocyte activation, leading to increased risk of cardiovascular events (death, stroke, and myocardial infarction) and higher coronary artery calcium scores (CACs). Vitamins D and K2 have significant anti-inflammatory effects; in addition, vitamin K2 is involved in preventing vascular calcifications in the general population. The roles of vitamins D and K in increased coronary calcifications in successfully treated PWH is less understood.We prospectively recruited 237 PWH on antiretroviral treatment (ART) and 67 healthy controls. CACs were derived from noncontrast chest computed tomography (CT) and levels of 25-hydroxyvitamin D (vitamin D) and inactive vitamin K-dependent dephosphorylated-uncarboxylated matrix Gla protein (dp-uc MGP, marker of vitamin K deficiency) were measured in plasma during a fasting state. The relationship between inflammation markers, dp-uc MGP, and vitamin D on CACs were estimated using zero-inflated negative binomial regression. Adjusted models included 25(OH)D, MGP, sex, race, age, and markers of inflammation or monocyte activation.Overall, controls had lower median age (45.8 vs. 48.8; P = 0.03), a larger proportion of female individuals (55.2 vs. 23.6%; P 0.0001), and nonwhite (33.8 vs. 70%; P 0.0001). Among PWH, less than 1% had detectable viral load and the median CD4+ cell count was 682 (IQR: 473.00-899.00). 62.17% of the participants had zero CACs and 51.32% were vitamin D-deficient (20 ng/ml). There was no difference in detectable CACs (P = 0.19) or dp-uc MGP (P = 0.42) between PWH and controls. In adjusted models, PWH with nonzero CACs have three times greater expected CAC burden compared with controls. Every 1% increase in MGP (worse K status) decreases the probability of having CACs equal to zero by 21.33% (P = 0.01). Evidence suggests that the effects of 25(OH)D and MGP are inflammation-mediated, specifically through sVCAM, TNF-αRI, and TNF-αRII.Vitamin K deficiency is a modifiable preventive factor against coronary calcification in PWH. Further research should determine whether vitamin K supplementation would reduce systemic inflammation, vascular calcification, and risk of cardiovascular events in PWH.

Background: People living with HIV (PLWH) experience increased inflammation, risk of cardiovascular (CV) events, and coronary artery calcium scores (CACs). In cross-sectional analyses, vitamins D and K have been associated with CACs and may have an anti-inflammatory effect. The anti-inflammatory effects of Vitamins D and K in successfully treated PLWH is less understood. Methods: We prospectively recruited 237 PLWH on antiretroviral treatment and 67 HIV- healthy controls. CACs were derived from non-contrast CT and levels of 25-hydroxyvitamin D (vitamin D) and inactive vitamin K dependent dephosphorylated-uncarboxylated matrix G1a protein (MGP, marker of vitamin K deficiency) were measured in plasma. The relationship between inflammation markers, MGP, and vitamin D on CACs were estimated using zero-inflated negative binomial regression. Adjusted models included 25(OH)D, MGP, gender, race, age, and markers of inflammation. Results: Controls had lower median age (45.8 vs. 48.8; p=0.03) and a larger proportion of females (55.2% vs. 23.6%; plog2 )25(OH)D is associated with >200% increase in the expected CACs among PLWH. Every one-unit increase in MGP (worse K status) decreases the probability of having CACs equal to zero 21.3% (p=0.01). Evidence suggests that the effects of 25(OH)D and MGP are inflammation mediated, specifically through VCAM and TNF-α pathways. Conclusion: Vitamins K deficiency is a modifiable preventive factor against coronary calcification in PLWH. Further research should determine whether vitamin K supplementation would reduce vascular calcification and risk of CV events in PLWH and increased inflammation

Background Diaphragmatic pacemakers are used to assist respiration in ventilator-dependent patients. Electromagnetic interference with intrinsic cardiac electrical activity is a theoretical risk but has never been reported in the literature. This case highlights a serious complication of cardiac arrest as a result of diaphragmatic pacing. Case summary We report a quadriplegic patient with recent diaphragmatic pacemaker implantation who presented with ventricular tachycardia leading to cardiac arrest. Extensive workup was negative for other aetiologies for ventricular arrhythmias. Reduction of the left-sided diaphragmatic pacemaker voltage resulted in cessation of ventricular ectopy. Discussion Diaphragmatic pacing at high voltages can cause unwanted transmission of impulses to the cardiac myocytes as a rare complication. This should be noted as a possible complication of intramuscular diaphragmatic pacing, and efforts should be taken to circumvent this risk in the future.

Patients with chronic kidney disease (CKD) are at increased risk for stroke. High-sensitivity troponin (hsTP), a marker of myocardial injury, has been associated with stroke risk in patients without CKD, but whether this applies to patients with CKD is not known. We assessed whether hsTP levels is associated with incident stroke in patients with mild-to-moderate CKD without a history of stroke enrolled in the Chronic Renal Insufficiency Cohort. Patients were followed for incident stroke, and the association with hsTP was assessed. A total of 3477 patients without prior stroke were included in this investigation. Over a median follow-up of 7.3 years, 101 (2.8%) patients had an incident stroke. Baseline hsTP was associated with a 9-year risk of stroke (quartile 1: 1.8%, quartile 2: 3.8%, quartile 3: 4.9%, quartile 4: 7.3%; P < .001). After adjusting for traditional stroke risk factors, patients in the fourth quartile (hazard ratio: 2.52, 95% CI: 1.10-5.76, P = .021) had higher risk of stroke when compared with the lowest quartile of hsTP. In conclusion, hsTP levels are associated with increased risk of incident stroke in patients with mild to moderate CKD, and this association remains significant despite the adjustment for traditional risk factors and CKD.

Penetrating cardiac trauma is one of the most critically challenging injuries with a devastating mortality if there is a delay in treatment or recognition. Despite a myriad of case reports of gunshot wounds to the left ventricle in trauma annals, there is a scarcity of reports in echocardiographic literature. We would like to describe a case report of a 35-year-old who presented after multiple gunshot wounds to the chest. He was taken emergently to the operating room for a pericardiotomy and repair of a laceration of the left ventricle, however no bullet fragment was found. On postoperative day six, the bullet was discovered via echocardiography to have migrated into the aortic root causing severe aortic insufficiency requiring return to the operating room, removal of the bullet, repair of the aorta and aortic valve, and was successfully discharged from the hospital on hospital day 14.

Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) support is an increasingly used temporizing therapy for patients with refractory cardiogenic shock. Contrast-enhanced echocardiography plays a critical role in the diagnosis and management of diseases that precipitate severe cardiac failure. In this case report, we describe a previously healthy 60-year-old woman who presented with dyspnea on exertion, and whose hospital course was complicated by ventricular fibrillation, emergent coronary artery bypass surgery (CABG), and ECMO support. Her contrast-enhanced ECMO images demonstrated a unique pattern of opacification of three of the four cardiac chambers, which led to a diagnosis of severe aortic insufficiency.