Cardiovascular (CV) disease is the leading cause of mortality in systemic lupus erythematosus (SLE). The risk of myocardial infarction (MI) in SLE is twice the incidence and ten years earlier in onset than in the general population. We present the first known case in the Philippines of acute MI from triple vessel coronary artery disease (CAD) in a young female patient with SLE. This aims to increase recognition and improve preventive strategies for this rare lupus complication. A 31-year-old female with SLE for thirteen years, antiphopspholipid syndrome (APS) and controlled hypertension (HTN) presented with acute chest pain, diaphoresis, and dyspnea. She was a non-smoker with quiescent lupus and nephritis, maintained on low-dose aspirin, mycophenolate mofetil and hydroxychloroquine for the past four years. The physical examination revealed hypertension, bradycardia, normal heart sounds without murmurs, and no signs of lupus flare. The troponin level was elevated, and the electrocardiogram showed inferior wall ST-segment elevation myocardial infarction (STEMI). Coronary angiography revealed triple-vessel disease, with 80-90% stenosis of the left circumflex artery, and total occlusion of the left anterior descending and right coronary artery. There were segmental wall motion abnormalities and a low ejection fraction of 44% on echocardiography. The complete blood count, urinalysis, and serum C3 were within normal range. The anti-dsDNA was low and lipid levels were abnormal. The patient refused coronary artery bypass grafting (CABG). Medical management consisting of anti-platelets, beta-blockers, statin, and warfarin was maximized. The patient completed one year of follow-up without any lupus flares or cardiovascular events. This case illustrates the complex interaction of disease-related and traditional cardiovascular risk factors leading to premature coronary artery disease in a young female with SLE. The case demonstrates favorable one-year outcomes after optimized post-MI medical management. Aside from optimized lupus control and reduced glucocorticoid use, proactive screening and aggressive management of modifiable CV risk factors and antiphospholipid antibodies (aPL), are necessary.
Human ; Female ; Adult: 25-44 Yrs Old ; Lupus Erythematosus, Systemic ; Myocardial Infarction ; Literature ; Infarction ; Female

INTRODUCTION

Acute coronary syndrome (ACS) and end-stage renal disease (ESRD) are both prevalent globally. The diagnosis and management of ACS in ESRD is difficult because the interplay of cardiovascular and renal disease is complicated. The guidelines for ACS may not be applicable to the ESRD population because the trials from which these are drawn mostly excluded ESRD patients.

To determine the clinical profile and outcomes of CKD patients on dialysis admitted for ACS in the Philippine General Hospital (PGH).

We did a retrospective cohort study and employed a retrospective review of electronic medical records among ESRD patients presenting with ACS in PGH from May 2021 to November 2023. The collected data was analyzed using univariate and bivariate statistics using PRISM software.

A total of 48 patients with ESRD were admitted for ACS in this study – 8 with STEMI and 40 with NSTEMI. The mean age was 61 years old and 33 (68.8%) were male. Among those with STEMI, six (75%) presented with Kilip II or more. While among those with NSTEMI, 17 (42.5%) had a GRACE score >140 and 27 (67.5%) had an NSTEMI TIMI risk score >2. On average, the patients were on hemodialysis for 31 months prior to admission. The most common comorbidities were hypertension (91.7%) and heart failure (83.3%). On admission, 18 (37.5%) presented with SBP >160, 7 (14.6%) patients presented with shock, and 4 (8.3%) patients presented with cardiac arrest. 38 (79.2%) patients had anemia on admission. 21 (43.8%) patients had left ventricular hypertrophy on electrocardiogram while 34 (70.8%) patients had cardiomegaly on chest radiography. The average left ventricular ejection fraction on echocardiogram was 46% and 27 (90%) patients had segmental wall motion abnormalities. The most common angiographic finding was 3-vessel coronary artery disease seen in 50% of patients. Almost all patients received dualantiplatelet therapy, high dose statin, and beta-blocker. The mortality rate was high at 43.8% with cardiovascular causes being the most common cause of death.

This study demonstrates the high mortality rate among patients with ESRD presenting with ACS. Our study portrays that patients with ESRD present with higher risk features including abnormalities in vital signs, laboratories, imaging, high prognostications score, and high in-hospital morbidity.

INTRODUCTION

Takayasu arteritis (TA) is a rare chronic large vessel vasculitis that affects the aorta and its major branches with a median age of onset of 25 years. The disease has a worldwide incidence of 1-2 per million, primarily affecting females with a 9:1 ratio. It is considered as an autoimmune disease that leads to progressive vessel thickening and stenosis, or aneurysmal dilatation. Coronary artery involvement is observed in 5.9%-58.2% of TA cases. We present a case of TA in a Filipino male presenting concurrently with myocardial infarction (MI) and ischemic stroke.

A 41-year-old Filipino male smoker with hypertension presented with chest pain, left-sided paresthesia and hemiparesis. Initial assessment revealed differential blood pressure between the arms, sensory and motor deficits, and abnormal ABI. Electrocardiogram confirmed anteroseptal ST-elevation MI and cranial computed tomography (CT) showed ischemic stroke. Arterial duplex scan had findings suggestive of hemodynamically significant lower extremity stenosis. A CT aortogram revealed multiple occlusions, including in the left subclavian artery, suggesting TA. Coronary angiography was attempted but was deferred due to peripheral arterial occlusion. A CT coronary angiogram revealed severe stenosis of the left anterior descending artery and moderate stenosis of the other coronaries. The patient was treated with dual antiplatelet therapy, statins, anticoagulation, corticosteroids and methotrexate. He experienced significant improvement in neurological symptoms and was chest pain-free upon discharge. At the 1-month follow-up, the patient remained asymptomatic.

Coronary involvement in TA can manifest as angina, MI, or other coronary lesions. The coexistence of MI and ischemic stroke in the same event is rare. Traditional risk factors for ischemic heart disease (IHD) in this patient such as hypertension and smoking may have contributed to the presentation, though TA itself is known to accelerate atherosclerosis. Limited vascular access hindered coronary intervention in this case and revascularization strategies remain challenging in active TA. The formation of extensive collateral arteries, along with early initiation of immunosuppressive therapy, likely contributed to the patient’s survival.

This case illustrates a rare and complex case of TA in a male patient with concurrent MI and ischemic stroke. Although coronary revascularization was not pursued due to occluded access, immunosuppressive therapy successfully managed the patient’s condition. Extensive collateral artery formation and early therapeutic intervention were key factors in the patient’s favorable outcome.

INTRODUCTION

The existence of a coronary artery aneurysm (CAA) can pose significant risk for death. It can cause thrombosis, dissection, rupture or myocardial infarction. An exceedingly rare involvement of the left main coronary artery (LMCA), particularly giant-sized is even more catastrophic, a finding seen in only 0.1% of patients. Furthermore, co-existence with significant stenotic coronary artery disease (CAD) portends grim survival. Owing to the rarity of this combination, no data is available locally and only limited case reports are documented internationally. Hence, no consensus guidelines have been published yet. This paper aims to contribute to the sparse medical knowledge on the treatment approach and management of LMCA aneurysm with concomitant CAD.

A 62-year-old male, Filipino, hypertensive and hyperlipidemic sought consult due to one-year exertional chest pain. Coronary angiogram revealed the LMCA to be a diffusely aneurysmal, large-sized vessel measuring 9.7 mm x 7.9 mm with a significant two-vessel CAD affecting the proximal left anterior descending (LAD) and right coronary artery (RCA). As per multidisciplinary decision, the patient underwent surgical revascularization via cardiopulmonary bypass graft (CABG) addressing the CAD and LMCA aneurysm managed conservatively through guideline-directed medical therapy. The patient’s course of treatment was uneventful. He returned for follow-ups for three months post-surgery and remained symptom-free.

Giant coronary artery aneurysms (GCAA) are vessel dilatations that exceed 4x the diameter of a normal adjacent artery. The patient had a unique case of GCAA involving the LMCA combined with two-vessel CAD. Few studies have documented a medical or surgical approach and long-term outcomes are unknown. Without sufficient evidence-based guidelines, the multidisciplinary decision was to perform CABG and manage the LMCA aneurysm conservatively.

Due to extremely limited information available on the giant LMCA aneurysm natural history, definitive management remains controversial. A multidisciplinary team approach is highly recommended for patient-specific needs to achieve favorable outcome and ensure survival.

OBJECTIVE: To observe the degree of myocardial cell injury and the changes in autophagy level in rats with myocardial ischemia/reperfusion (I/R) injury induced by cardiopulmonary bypass (CPB), and to explore the regulatory role of the long non-coding RNA-urothelial carcinoma antigen 1-microRNA-143-Notch1 axis (lncRNA-UCA1-miR-143-Notch1 axis) in myocardial I/R injury induced by CPB. METHODS: Healthy male Sprague-Dawley (SD) rats were randomly divided into the following groups using the random number method: Sham operation (Sham) group, myocardial I/R injury model group (model group), empty lentivirus group, lncRNA-UCA1 upregulation group, miR-143 downregulation group, and lncRNA-UCA1 upregulation+miR-143 upregulation group, with 9 rats in each group. The rat model of myocardial I/R injury induced by CPB was established by thoracotomy aortic ligation under cardiopulmonary bypass support; in the Sham group, only threading was performed without ligation, and other procedures were the same. Seventy-two hours before modeling, the lncRNA-UCA1 upregulated group was injected with 100 μL of myocardial tissue-specific adeno-associated virus (AAV) overexpression vector of lncRNA-UCA1 via tail vein, the miR-143 downregulated group was injected with 100 μL of AAV short hairpin RNA (shRNA) vector of miR-143 via tail vein, the lncRNA-UCA1 upregulation+miR-143 upregulation group was injected with 100 μL of myocardial tissue-AAV overexpression vector of lncRNA-UCA1 and 100 μL of AAV overexpression vector of miR-143 via tail vein, and the empty vector lentivirus group was injected with 100 μL of AAV empty vector (virus titers were 1×10⁹ TU/mL); the Sham group and the model group were injected with equal amounts of normal saline. The animals were euthanized 24 hours after intervention and cardiac tissue specimens were collected. After hematoxylin eosin (HE) staining, the damage of myocardial cells and the changes of muscle fiber tissue were observed under a light microscope; after dual staining with uranyl acetate and lead citrate, the ultrastructural damage of heart tissue was observed under a transmission electron microscopy; the expression of lncRNA-UCA1, miR-143, and Notch1 mRNA in myocardial tissue was detected by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR); the expression of microtubule 1 light chain 3-II/I (LC3-II/I) and Notch1 protein in myocardial tissue was detected by Western blotting. RESULTS: Compared with the Sham group, the myocardial cells of rats in the model group were enlarged, the intercellular space increased, autophagosomes increased, the arrangement of myocardial fibers was disordered, mitochondrial proliferated and deformed. The expression levels of lncRNA-UCA1 and Notch1 mRNA, as well as the protein expression levels of LC3-II/I and Notch1 were significantly increased, while the expression level of miR-143 was significantly decreased. Compared with the model group, the degree of myocardial cell injury in the lncRNA-UCA1 upregulation group and miR-143 downregulation group was significantly alleviated, the expression levels of Notch1 mRNA, LC3-II/I, and Notch1 protein were significantly increased [Notch1 mRNA (2^-ΔΔCt): 2.66±0.24, 2.03±0.23 vs. 1.45±0.13, LC3-II/I: 2.10±0.21, 1.92±0.19 vs. 1.39±0.14, Notch1 protein (Notch1/GAPDH): 1.72±0.16, 1.57±0.16 vs. 1.34±0.13, all P < 0.05], and the expression level of miR-143 was significantly decreased (2^-ΔΔCt: 0.50±0.06, 0.52±0.06 vs.0.71±0.06, P < 0.05). The expression level of lncRNA-UCA1 in the lncRNA-UCA1 upregulated group was significantly higher than that in the model group (2^-ΔΔCt: 2.47±0.22 vs. 1.43±0.14, P < 0.05), while there was no significant difference in the miR-143 downregulation group compared with the model group (2^-ΔΔCt: 1.50±0.16 vs. 1.43±0.14, P > 0.05). There was no significant difference in the degree of myocardial cell injury in the empty load lentivirus group and the lncRNA-UCA1 upregulation+miR-143 upregulation group compared to the model group. There were no significant differences in the expression of miR-143, Notch1 mRNA, and the autophagy level in these two groups compared to the model group. The expression level of lncRNA-UCA1 in the lncRNA-UCA1 upregulation+miR-143 upregulation group was significantly higher than that in the model group (2^-ΔΔCt: 2.47±0.20 vs. 1.43±0.14, P < 0.05). CONCLUSIONS Autophagy is involved in the pathological process of myocardial I/R injury induced by CPB. The lncRNA-UCA1-microRNA-143-Notch1 axis may regulate the autophagy level to participate in the I/R injury process.
Animals ; MicroRNAs ; Rats, Sprague-Dawley ; RNA, Long Noncoding ; Male ; Myocardial Reperfusion Injury/etiology* ; Rats ; Cardiopulmonary Bypass/adverse effects* ; Receptor, Notch1/metabolism* ; Autophagy

Tianxiangdan (TXD), a traditional Chinese herbal remedy, demonstrates efficacy in mitigating myocardial ischemia-reperfusion (I/R)-induced damage. This study employed network pharmacology to evaluate the therapeutic targets and mechanisms of TXD in treating I/R. High-performance liquid chromatography-mass spectrometry (HPLC-MS) identified 86 compounds in TXD. Network pharmacological analysis predicted potential target genes and their modes of action. Cardiac function, ischaemic ST changes, lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) activity, myocardial fiber, and infarct size were assessed using in vivo and in vitro I/R injury models. Estrogen receptor alpha (ERα) protein expression and estradiol (E2) levels were measured to confirm TXD's impact on estrogen levels and ERα expression. To examine if TXD reduces I/R injury through ERα, an AZD group (300 nmol·L^-1 AZD9496 and 15% TXD serum) was compared to a TXD group (15% TXD serum). The study hypothesized that TXD upregulates the ERα-mediated iron metamorphosis pathway. I/R injury-induced ferroptosis was identified using a Fer-1 group (1.0 μmol·L^-1 Fer-1 and 15% TXD serum) to elucidate the potential association between ferroptosis and ERα proteins. A DCFH-DA probe detected reactive oxygen species (ROS) and Fe²⁺, while Western blotting assessed target protein expression. Both in vitro and in vivo experiments demonstrated that TXD attenuated I/R injury by reducing elevated ST-segment levels, improving cardiac injury biomarkers (LDH, MDA, and SOD), alleviating pathological features, and preventing I/R-induced loss of cell viability in vitro. The effects and mechanisms of TXD on I/R injury-associated ferroptosis were investigated using I/R-induced H9c2 cells. The TXD group showed significantly decreased ROS and Fe²⁺ levels, while the AZ group (treated with AZD9496) exhibited increased levels. The TXD group demonstrated enhanced expression of ERα and glutathione peroxidase 4 (GPX4), with reduced levels of P53 protein and ferritin-heavy polypeptide 1 (FTH1). The AZ group exhibited contrasting effects on these expression levels. The literature indicated a novel connection between ERα and ferroptosis. TXD activates the ERα signaling pathway, promoting protection against I/R-induced myocardial cell ferroptosis. This study provides evidence supporting TXD use for myocardial ischemia treatment, particularly in older female patients who may benefit from its therapeutic outcomes.
Animals ; Ferroptosis/drug effects* ; Estrogen Receptor alpha/genetics* ; Myocardial Reperfusion Injury/genetics* ; Drugs, Chinese Herbal/pharmacology* ; Male ; Mice ; Humans ; Mice, Inbred C57BL ; Estradiol/metabolism*

Myocardial infarction is a cardiovascular disease (CVD) with high morbidity and mortality, which can trigger a cascade of cardiac pathophysiological changes, including fibrosis, inflammation, ischemia-reperfusion injury (IRI), and ventricular remodeling, ultimately leading to heart failure (HF). While conventional pharmacological treatments and clinical reperfusion therapy may enhance short-term prognoses and emergency survival rates, both approaches have limitations and adverse effects. Natural products (NPs) are extensively utilized as therapeutics globally, with some demonstrating potentially favorable therapeutic effects in preclinical and clinical pharmacological studies, positioning them as potential alternatives to modern drugs. This review comprehensively elucidates the pathophysiological mechanisms during myocardial infarction and summarizes the mechanisms by which NPs exert cardiac beneficial effects. These include classical mechanisms such as inhibition of inflammation and oxidative stress, alleviation of cardiomyocyte death, attenuation of cardiac fibrosis, improvement of angiogenesis, and emerging mechanisms such as cardiac metabolic regulation and histone modification. Furthermore, the review emphasizes the modulation by NPs of novel targets or signaling pathways in classical mechanisms, including other forms of regulated cell death (RCD), endothelial-mesenchymal transition, non-coding ribonucleic acids (ncRNAs) cascade, and endothelial progenitor cell (EPC) function. Additionally, NPs influencing a particular mechanism are categorized based on their chemical structure, and their relevance is discussed. Finally, the current limitations and prospects of NPs therapy are considered, highlighting their potential for use in myocardial infarction management and identifying issues that require urgent attention.
Humans ; Myocardial Infarction/genetics* ; Biological Products/therapeutic use* ; Animals ; Oxidative Stress/drug effects* ; Signal Transduction/drug effects*

Sini Decoction (SNT) is a traditional formula recognized for its efficacy in warming the spleen and stomach and dispersing cold. However, elucidating the mechanism of action of SNT remains challenging due to its complex multiple components. This study utilized a synergistic approach combining two-dimensional fluorescence difference in gel electrophoresis (2D-DIGE)-based drug affinity responsive target stability (DARTS) with label-free quantitative proteomics techniques to identify the direct and indirect protein targets of SNT in myocardial infarction. The analysis identified 590 proteins, with 30 proteins showing significant upregulation and 51 proteins showing downregulation when comparing the SNT group with the model group. Through the integration of 2D-DIGE DARTS with proteomics data and pharmacological assessments, the findings indicate that protein disulfide-isomerase A3 (PDIA3) may serve as a potential protein target through which SNT provides protective effects on myocardial cells during myocardial infarction.
Myocardial Infarction/genetics* ; Proteomics/methods* ; Drugs, Chinese Herbal/chemistry* ; Animals ; Protein Disulfide-Isomerases/genetics* ; Male ; Two-Dimensional Difference Gel Electrophoresis/methods* ; Humans ; Rats ; Rats, Sprague-Dawley ; Electrophoresis, Gel, Two-Dimensional

Coronary artery disease (CAD), one of the most common cardiovascular diseases (CVD), poses a serious threat to physical and mental health, resulting in a severe disease burden. Psychocardiology medicine focuses on the vital role of psychological factors in the development, diagnosis, and treatment of CVD. The prevalence of depression and anxiety is high in patients with CAD. Furthermore, there is a vital interplay among depression, anxiety, mental stress-induced myocardial ischemia, cognitive impairment, and delirium. Both cognitive impairment and delirium adversely impact the prognosis of patients with CAD, warranting increasing attention and the development of interventions. To further direct the clinic diagnosis and treatment of cognitive impairment in patients with CAD complicated with depression and anxiety, and to thus improve the prognosis of such patients, the Psychocardiology Medicine Branch of Chinese Medical Association Beijing Branch, and Psychocardiology Education Professional Committee of China Medical Education Association, together with over 40 other organizations, including more than 50 experts from several related fields, have developed the association standards on guidelines for the cognitive clinical diagnosis and treatment of CAD complicated with depression and anxiety under the framework of the China standard association (No.T/CAS 812-2024).
Humans ; Depression/diagnosis* ; Coronary Artery Disease/psychology* ; Anxiety/diagnosis* ; Practice Guidelines as Topic

OBJECTIVE: This study aimed to investigate the impact of glycemic control and diabetes duration on subsequent myocardial infarction (MI) in patients with both coronary heart disease (CHD) and type 2 diabetes (T2D). METHODS: We conducted a retrospective cohort study of 33,238 patients with both CHD and T2D in Shenzhen, China. Patients were categorized into 6 groups based on baseline fasting plasma glucose (FPG) levels and diabetes duration (from the date of diabetes diagnosis to the baseline date) to examine their combined effects on subsequent MI. Cox proportional hazards regression models were used, with further stratification by age, sex, and comorbidities to assess potential interactions. RESULTS: Over a median follow-up of 2.4 years, 2,110 patients experienced MI. Compared to those with optimal glycemic control (FPG < 6.1 mmol/L) and shorter diabetes duration (< 10 years), the fully-adjusted hazard ratio ( HR) (95% Confidence Interval [95% CI]) for those with a diabetes duration of ≥ 10 years and FPG > 8.0 mmol/L was 1.93 (95% CI: 1.59, 2.36). The combined effects of FPG and diabetes duration on MI were largely similar across different age, sex, and comorbidity groups, although the excess risk of MI associated with long-term diabetes appeared to be more pronounced among those with atrial fibrillation. CONCLUSION Our study indicates that glycemic control and diabetes duration significant influence the subsequent occurrence of MI in patients with both CHD and T2D. Tailored management strategies emphasizing strict glycemic control may be particularly beneficial for patients with longer diabetes duration and atrial fibrillation.
Humans ; Diabetes Mellitus, Type 2/blood* ; Male ; Female ; Middle Aged ; Aged ; Coronary Disease/complications* ; Myocardial Infarction/etiology* ; Retrospective Studies ; China/epidemiology* ; Glycemic Control ; Blood Glucose ; Adult ; Risk Factors ; Time Factors