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Journal of Cardiovascular Development... Sep 2023The clinical presentation of pulmonary embolism (PE) and acute coronary syndrome can be similar. We report a case of a patient presenting with antero-septal ST-segment...
The clinical presentation of pulmonary embolism (PE) and acute coronary syndrome can be similar. We report a case of a patient presenting with antero-septal ST-segment elevation after cardiac arrest, found to have acute-PE-mimicking ST-segment elevation myocardial infarction (STEMI), treated with aspiration thrombectomy and catheter-directed thrombolysis (CDT). A 78-year-old man was admitted with dyspnea, chest pain and tachycardia. During evaluation, cardiac arrest in pulseless electrical activity was documented. Advanced life support was started immediately. ECG post-ROSC revealed ST-segment elevation in V1-V4 and aVR. Echocardiography showed normal left ventricular function but right ventricular (RV) dilation and severe dysfunction. The patient was in shock and was promptly referred to cardiac catheterization that excluded significant CAD. Due to the discordant ECG and echocardiogram findings, acute PE was suspected, and immediate invasive pulmonary angiography revealed bilateral massive pulmonary embolism. Successful aspiration thrombectomy was performed followed by local alteplase infusion. At the end of the procedure, mPAP was reduced and blood pressure normalized allowing withdrawal of vasopressor support. Twenty-four-hour echocardiographic reassessment showed normal-sized cardiac chambers with preserved biventricular systolic function. Bedside echocardiography in patients with ST-segment elevation post-ROSC is instrumental in raising the suspicion of acute PE. In the absence of a culprit coronary lesion, prompt pulmonary angiography should be considered if immediately feasible. In these cases, CDT and aspiration in high-risk acute PE seem safe and effective in relieving obstructive shock and restoring hemodynamics.
PubMed: 37754803
DOI: 10.3390/jcdd10090374 -
Frontiers in Oncology 2023Clonal hematopoiesis of indeterminate potential (CHIP) has fascinated the medical community for some time. Discovered about a decade ago, this phenomenon links... (Review)
Review
Clonal hematopoiesis of indeterminate potential (CHIP) has fascinated the medical community for some time. Discovered about a decade ago, this phenomenon links age-related alterations in hematopoiesis not only to the later development of hematological malignancies but also to an increased risk of early-onset cardiovascular disease and some other disorders. CHIP is detected in the blood and is characterized by clonally expanded somatic mutations in cancer-associated genes, predisposing to the development of hematologic neoplasms such as MDS and AML. CHIP-associated mutations often involve DNA damage repair genes and are frequently observed following prior cytotoxic cancer therapy. Genetic predisposition seems to be a contributing factor. It came as a surprise that CHIP significantly elevates the risk of myocardial infarction and stroke, and also contributes to heart failure and pulmonary hypertension. Meanwhile, evidence of mutant clonal macrophages in vessel walls and organ parenchyma helps to explain the pathophysiology. Besides aging, there are some risk factors promoting the appearance of CHIP, such as smoking, chronic inflammation, chronic sleep deprivation, and high birth weight. This article describes fundamental aspects of CHIP and explains its association with hematologic malignancies, cardiovascular disorders, and other medical conditions, while also exploring potential progress in the clinical management of affected individuals. While it is important to diagnose conditions that can lead to adverse, but potentially preventable, effects, it is equally important not to stress patients by confronting them with disconcerting findings that cannot be remedied. Individuals with diagnosed or suspected CHIP should receive counseling in a specialized outpatient clinic, where professionals from relevant medical specialties may help them to avoid the development of CHIP-related health problems. Unfortunately, useful treatments and clinical guidelines for managing CHIP are still largely lacking. However, there are some promising approaches regarding the management of cardiovascular disease risk. In the future, strategies aimed at restoration of gene function or inhibition of inflammatory mediators may become an option.
PubMed: 38162500
DOI: 10.3389/fonc.2023.1303785 -
Cell Biology and Toxicology Mar 2024Cardiovascular diseases (CVDs) are the main diseases that endanger human health, and their risk factors contribute to high morbidity and a high rate of hospitalization.... (Review)
Review
Cardiovascular diseases (CVDs) are the main diseases that endanger human health, and their risk factors contribute to high morbidity and a high rate of hospitalization. Cell death is the most important pathophysiology in CVDs. As one of the cell death mechanisms, ferroptosis is a new form of regulated cell death (RCD) that broadly participates in CVDs (such as myocardial infarction, heart transplantation, atherosclerosis, heart failure, ischaemia/reperfusion (I/R) injury, atrial fibrillation, cardiomyopathy (radiation-induced cardiomyopathy, diabetes cardiomyopathy, sepsis-induced cardiac injury, doxorubicin-induced cardiac injury, iron overload cardiomyopathy, and hypertrophic cardiomyopathy), and pulmonary arterial hypertension), involving in iron regulation, metabolic mechanism and lipid peroxidation. This article reviews recent research on the mechanism and regulation of ferroptosis and its relationship with the occurrence and treatment of CVDs, aiming to provide new ideas and treatment targets for the clinical diagnosis and treatment of CVDs by clarifying the latest progress in CVDs research.
Topics: Humans; Cardiovascular Diseases; Ferroptosis; Myocardial Infarction; Cell Death; Cardiomyopathies
PubMed: 38509409
DOI: 10.1007/s10565-024-09853-w -
The Egyptian Heart Journal : (EHJ) :... Sep 2023Congenital pericardial absence is an uncommon cardiac anomaly that is typically asymptomatic and commonly misdiagnosed due to a lack of symptoms or atypical symptoms....
BACKGROUND
Congenital pericardial absence is an uncommon cardiac anomaly that is typically asymptomatic and commonly misdiagnosed due to a lack of symptoms or atypical symptoms. Pericardial agenesis (PA) should be considered one of the differential diagnoses when the patient presents with chest pain. This case shows how the diagnosis of pericardial agenesis is made exclusively using multi-modality imaging, starting from findings in a basic chest radiograph to cardiac MRI, while also demonstrating the classic signs seen in this condition. Magnetic resonance imaging of the heart is the gold standard for determining the absence of pericardium in the prognosis.
CASE PRESENTATION
A 32-year-old male who presented with chest discomfort and radiating pain to his back and left shoulder mimicking myocardial infarction with normal ECG and enzyme markers. A chest radiograph (taken 24 h apart) demonstrates the left lateral position of the heart and the bulging contour of the left heart border, a lucent area between the aorta and pulmonary artery. Subsequently, cardiac MRI reveals left pericardial agenesis.
CONCLUSIONS
This article provides insight into a rare differential to consider in a young patient presenting with chest discomfort. This case shows how the diagnosis of pericardial agenesis is made exclusively using multi-modality imaging, starting from findings in a basic chest radiograph to cardiac MRI, while also demonstrating the classic signs seen in this condition.
PubMed: 37725161
DOI: 10.1186/s43044-023-00405-x -
Journal of Education & Teaching in... Jul 2023Emergency medicine residents and medical students on emergency medicine rotation.
AUDIENCE
Emergency medicine residents and medical students on emergency medicine rotation.
INTRODUCTION
Acute pulmonary edema is a common and potentially fatal presentation in the emergency department. More than 1 million patients are admitted annually with a diagnosis of pulmonary edema secondary to cardiac causes.1 Pulmonary edema is broadly split into two main categories: cardiogenic and noncardiogenic. Cardiogenic pulmonary edema is characterized by acute dyspnea caused by the accumulation of fluid within the lung's interstitial and/or alveolar spaces, which is the result of acutely elevated cardiac filling pressures.2 Noncardiogenic pulmonary edema is characterized by fluid accumulation within the alveolar space in the absence of elevated pulmonary capillary wedge pressure.2 These patients often present critically ill, and rapid identification and aggressive management is paramount in caring for patients with pulmonary edema. Dyspnea is the most common presentation with a sensitivity of 89% but a low specificity of 51%.3 Workup of pulmonary edema often includes laboratory testing, electrocardiogram (EKG), chest x-ray (CXR), and often bedside ultrasound (US) and echocardiography.4 Pulmonary edema management depends on the etiology but is often focused on preload and afterload reduction. Diuretics, nitrates, and optimizing ventilatory support through non-invasive and invasive strategies are the mainstay of treatment.
EDUCATIONAL OBJECTIVES
At the end of this practice oral boards case, the learner will:1) recognize unstable vital signs (VS) and intervene to stabilize ventilation and oxygenation, 2) demonstrate the ability to obtain a complete medical history including the important characteristics of chest pain, 3) demonstrate an appropriate exam on a patient, 4) order the appropriate evaluation studies for a patient with complaints of dyspnea, 5) interpret the results of diagnostic evaluation and diagnose Non- ST elevation myocardial infarction (NSTEMI) and pulmonary edema, 6) order appropriate management of pulmonary edema and NSTEMI, and 6) demonstrate effective communication with patient and family members.
EDUCATIONAL METHODS
Practice oral boards.
RESEARCH METHODS
Immediate Feedback was solicited from the learners and observers participating in the case both by verbal discussion and completion of a rating for the case following the debriefing. The efficacy of the educational content was assessed by comparing scoring measures across residents based on the training year. Scoring measures of the American College of Graduate Medical Education (ACGME) core competencies were performed using a scale from 1 - 8, 1-4 being unacceptable performance and 5 - 8 being acceptable. Efficacy was assumed based on full completion of the case by the residents who acted as practice oral board candidates, and a debriefing session followed to discuss the key components of the case.
RESULTS
This case was presented to twelve Emergency Medicine Residents, seven PGY 1 and five PGY 2 at a relatively new residency program. The overall average score for the residents was 5.62. The PGY 1 Residents' average on the case was 5.56, and the average for the PGY 2 Residents was slightly better at 5.70. The slight improvement noted by the PGY 2 Residents is likely attributable to more clinical experience; however, both classes did not have any prior exposure to the oral board format until this simulated experience. Six residents completed all critical actions in the case. Of those who missed a critical action, failing to diagnose NSTEMI and consulting cardiology were the most common. All learners found educational value in the case with an overall rating of 4.83 (1-5 Likert scale, 5 being excellent).
DISCUSSION
Acute pulmonary edema and NSTEMI are common diagnoses that will be frequently encountered for most emergency physicians. This case highlights the need for early identification and aggressive management of the patient presenting with respiratory distress. The differential for respiratory distress is large, but most learners were able to quickly identify pulmonary edema based on the exam findings of jugular vein distention (JVD), rales, and lower extremity edema. Most learners quickly escalated to a non-rebreather mask and ultimately to BPAP (bilevel positive airway pressure) without requesting to intubate the patient. There was notable variation in the approach to administering nitrates, but most ordered an intravenous (IV) nitroglycerin (NTG) drip and requested pharmacy assistance in dosing. Diuretics were ordered by all the learners, but some were hesitant to start early because they felt the effect would be delayed. Some of the residents did not identify ischemic changes on the EKG at first glance but did request to review a second time when the troponin result was positive. All residents gave aspirin after noting the positive troponin, but not all were able to make a clear diagnosis of NSTEMI or consult cardiology. Although the case was relatively straightforward, residents enjoyed early diagnosis and aggressive management of the patient with impending respiratory failure. Many residents are asking for an ultrasound early in the workup of this patient presenting in respiratory distress. Although not a critical action in this case, it highlights the emphasis placed on ultrasonography in the current emergency medicine curriculum.
TOPICS
Pulmonary Edema, Cardiovascular emergencies, NSTEMI.
PubMed: 37575411
DOI: 10.21980/J8CW67 -
Journal of Clinical and Translational... Oct 2023Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Recently, accumulating evidence has revealed hepatic mediators, termed as... (Review)
Review
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Recently, accumulating evidence has revealed hepatic mediators, termed as liver-derived secretory factors (LDSFs), play an important role in regulating CVDs such as atherosclerosis, coronary artery disease, thrombosis, myocardial infarction, heart failure, metabolic cardiomyopathy, arterial hypertension, and pulmonary hypertension. LDSFs presented here consisted of microbial metabolite, extracellular vesicles, proteins, and microRNA, they are primarily or exclusively synthesized and released by the liver, and have been shown to exert pleiotropic actions on cardiovascular system. LDSFs mainly target vascular endothelial cell, vascular smooth muscle cells, cardiomyocytes, fibroblasts, macrophages and platelets, and further modulate endothelial nitric oxide synthase/nitric oxide, endothelial function, energy metabolism, inflammation, oxidative stress, and dystrophic calcification. Although some LDSFs are known to be detrimental/beneficial, controversial findings were also reported for many. Therefore, more studies are required to further explore the causal relationships between LDSFs and CVDs and uncover the exact mechanisms, which is expected to extend our understanding of the crosstalk between the liver and cardiovascular system and identify potential therapeutic targets. Furthermore, in the case of patients with liver disease, awareness should be given to the implications of these abnormalities in the cardiovascular system. These studies also underline the importance of early recognition and intervention of liver abnormalities in the practice of cardiovascular care, and a multidisciplinary approach combining hepatologists and cardiologists would be more preferable for such patients.
PubMed: 37577236
DOI: 10.14218/JCTH.2022.00122 -
American Journal of Physiology. Heart... Feb 2024Pulmonary and systemic congestion as a consequence of heart failure are clinically recognized as alarm signals for clinical outcome and mortality. Although signs and...
Pulmonary and systemic congestion as a consequence of heart failure are clinically recognized as alarm signals for clinical outcome and mortality. Although signs and symptoms of congestion are well detectable in patients, monitoring of congestion in small animals with heart failure lacks adequate noninvasive methodology yet. Here, we developed a novel ultrasonography-based scoring system to assess pulmonary and systemic congestion in experimental heart failure, by using lung ultrasound (LUS) and imaging of the inferior vena cava (Cava), termed CavaLUS. CavaLUS was established and tested in a rat model of supracoronary aortic banding and a mouse model of myocardial infarction, providing high sensitivity and specificity while correlating to numerous parameters of cardiac performance and disease severity. CavaLUS, therefore, provides a novel comprehensive tool for experimental heart failure in small animals to noninvasively assess congestion. As thorough, noninvasive assessment of congestion is not available in small animals, we developed and validated an ultrasonography-based research tool to evaluate pulmonary and central venous congestion in experimental heart failure models.
Topics: Humans; Mice; Animals; Rats; Hyperemia; Lung; Ultrasonography; Heart Failure; Vena Cava, Inferior
PubMed: 38099848
DOI: 10.1152/ajpheart.00735.2023 -
Asian Journal of Andrology Oct 2023To evaluate the relationship between testosterone replacement therapy (TRT) and arterial and/or venous thrombosis in patients with pre-treatment total testosterone (TT)...
To evaluate the relationship between testosterone replacement therapy (TRT) and arterial and/or venous thrombosis in patients with pre-treatment total testosterone (TT) <12 nmol l-1, we performed a meta-analysis following the Population Intervention Comparison Outcome model. Population: men with TT <12 nmol l-1 or clear mention of hypogonadism in the inclusion criteria of patients; intervention: TRT; comparison: placebo or no therapy; outcomes: arterial thrombotic events (stroke, myocardial infarction [MI], upper limbs, and lower limbs), VTE (deep vein thrombosis [DVT], portal vein thrombosis, splenic thrombosis, and pulmonary embolism), and mortality. A total of 2423 abstracts were assessed for eligibility. Twenty-four studies, including 14 randomized controlled trials (RCTs), were finally included, with a total of 4027 and 310 288 hypotestosteronemic male patients, from RCTs and from observational studies, respectively. Based on RCT-derived data, TRT did not influence the risk of arterial thrombosis (odds ratio [OR] = 1.27, 95% confidence interval [CI]: 0.47-3.43, P = 0.64), stroke (OR = 1.34, 95% CI: 0.09-18.97, P = 0.83), MI (OR = 0.51, 95% CI: 0.11-2.31, P = 0.39), VTE (OR = 1.42, 95% CI: 0.22-9.03, P = 0.71), pulmonary embolism (OR = 1.38, 95% CI: 0.27-7.04, P = 0.70), and mortality (OR = 0.70, 95% CI: 0.20-2.38, P = 0.56). Meanwhile, when only observational studies are considered, a significant reduction in the risk of developing arterial thrombotic events, MI, venous thromboembolism, and mortality was observed. The risk for DVT remains uncertain, due to the paucity of RCT-based data. TRT in men with TT <12 nmol l-1 is safe from the risk of adverse cardiovascular events. Further studies specifically assessing the risk of DVT in men on TRT are needed.
PubMed: 37921515
DOI: 10.4103/aja202352 -
Circulation Jun 2024Sodium-glucose cotransporter-2 inhibitors (SGLT2i) consistently improve heart failure and kidney-related outcomes; however, effects on major adverse cardiovascular... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) consistently improve heart failure and kidney-related outcomes; however, effects on major adverse cardiovascular events (MACE) across different patient populations are less clear.
METHODS
This was a collaborative trial-level meta-analysis from the SGLT2i Meta-analysis Cardio-Renal Trialists Consortium, which includes all phase 3, placebo-controlled, outcomes trials of SGLT2i across 3 patient populations (patients with diabetes at high risk for atherosclerotic cardiovascular disease, heart failure [HF], or chronic kidney disease). The outcomes of interest were MACE (composite of cardiovascular death, myocardial infarction , or stroke), individual components of MACE (inclusive of fatal and nonfatal events), all-cause mortality, and death subtypes. Effect estimates for SGLT2i versus placebo were meta-analyzed across trials and examined across key subgroups (established atherosclerotic cardiovascular disease, previous myocardial infarction, diabetes, previous HF, albuminuria, chronic kidney disease stages, and risk groups).
RESULTS
A total of 78 607 patients across 11 trials were included: 42 568 (54.2%), 20 725 (26.4%), and 15 314 (19.5%) were included from trials of patients with diabetes at high risk for atherosclerotic cardiovascular disease, HF, or chronic kidney disease, respectively. SGLT2i reduced the rate of MACE by 9% (hazard ration [HR], 0.91 [95% CI, 0.87-0.96], <0.0001) with a consistent effect across all 3 patient populations (=0%) and across all key subgroups. This effect was primarily driven by a reduction in cardiovascular death (HR, 0.86 [95% CI, 0.81-0.92], <0.0001), with no significant effect for myocardial infarction in the overall population (HR, 0.95 [95% CI, 0.87-1.04], =0.29), and no effect on stroke (HR, 0.99 [95% CI, 0.91-1.07], =0.77). The benefit for cardiovascular death was driven primarily by reductions in HF death and sudden cardiac death (HR, 0.68 [95% CI, 0.46-1.02] and HR, 0.86 [95% CI, 0.78-0.95], respectively) and was generally consistent across subgroups, with the possible exception of being more apparent in those with albuminuria (=0.02).
CONCLUSIONS
SGLT2i reduce the risk of MACE across a broad range of patients irrespective of atherosclerotic cardiovascular disease, diabetes, kidney function, or other major clinical characteristics at baseline. This effect is driven primarily by a reduction of cardiovascular death, particularly HF death and sudden cardiac death, without a significant effect on myocardial infarction in the overall population, and no effect on stroke. These data may help inform selection for SGLT2i therapies across the spectrum of cardiovascular-kidney-metabolic disease.
Topics: Sodium-Glucose Transporter 2 Inhibitors; Humans; Cardiovascular Diseases; Renal Insufficiency, Chronic; Diabetes Mellitus, Type 2; Female; Male; Treatment Outcome; Aged
PubMed: 38583093
DOI: 10.1161/CIRCULATIONAHA.124.069568 -
International Journal of Molecular... Jun 2024This review explores the intricate relationship between generalized pustular psoriasis (GPP) and various systemic diseases, shedding light on the broader impacts of this... (Review)
Review
This review explores the intricate relationship between generalized pustular psoriasis (GPP) and various systemic diseases, shedding light on the broader impacts of this severe skin condition beyond its primary dermatological manifestations. GPP is identified as not only a profound contributor to skin pathology but also a significant risk factor for systemic diseases affecting cardiovascular, hepatic, renal, pulmonary, and skeletal systems, as well as associated with an increased incidence of anemia, depression, anxiety, and arthritis. The research highlights the complex interplay of cytokines, particularly IL-17 and IL-36, which are central to the pathophysiology of GPP and implicated in the exacerbation of systemic conditions. Key findings indicate a higher incidence of cardiovascular events in GPP patients compared to those with other severe forms of psoriasis, notably with a stronger correlation between myocardial infarction history and GPP development. Liver disturbances, frequently reversible upon psoriasis remission, suggest a cytokine-mediated link to hepatic health. Renal dysfunction appears elevated in GPP sufferers, with IL-17 and IL-36 potentially driving renal fibrosis. Similarly, interstitial lung disease and osteoporosis in GPP patients underscore the systemic reach of inflammatory processes initiated in the skin. The associations with anemia, depression, anxiety, and arthritis further complicate the clinical management of GPP, requiring a multidisciplinary approach. The study concludes that managing GPP effectively requires a holistic approach that addresses both the cutaneous and systemic dimensions of the disease, advocating for continued research into the mechanisms that connect GPP with broader health implications to refine therapeutic strategies.
Topics: Humans; Psoriasis; Cytokines; Cardiovascular Diseases
PubMed: 38892457
DOI: 10.3390/ijms25116270