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Key Clinical Message Neglected rheumatic heart disease (RHD) can lead to severe complications and change patients' quality of life, particularly that of young patients. This report highlights the importance of public health education for patients and families in preventing RHD complications. In RHD management, prevention is better than cure.

Thyrotoxicosis is a common condition that is associated with cardiovascular complications. The most common complications that occurs are heart failure and cardiac arrhythmias. Cardiac arrhythmias due to thyrotoxicosis negatively affect the cardiovascular system at the cellular and molecular levels. The commonest cardiac arrhythmias are sinus tachycardia and atrial fibrillation. Left bundle branch block as a presentation of thyrotoxicosis is rare. We are reporting a case of a patient with a transient left bundle branch block as a thyrotoxicosis manifestation that was resolved after the thyroid status was normalized.

Abstract Background Differential polarization of macrophage into M1 and M2 mediates atherosclerotic plaque clearance through efferocytosis. Higher expression of Mer proto-oncogene tyrosine kinase (MerTK) on M2 macrophage helps in maintaining macrophage efferocytic efficiency. In healthy individuals, macrophage polarization into M1 and M2 occurs in tissues in concomitance with the acquisition of functional phenotypes depending on specific microenvironment stimuli. However, whether the macrophage differential polarization and MerTK expression vary in coronary artery disease (CAD) patients remain unknown. Objective This study aimed to elucidate the polarization of M1 and M2 macrophage from CAD patients as well as to investigate the expression of MerTK in these macrophage phenotypes. Methods A total of 14 (n) CAD patients were recruited and subsequently grouped into “no apparent CAD”, “non-obstructive CAD” and “obstructive CAD” according to the degree of stenosis. Thirty ml of venous blood was withdrawn to obtain monocyte from the patients. The M1 macrophage was generated by treating the monocyte with GMCSF, LPS and IFN-γ while MCSF, IL-4 and IL-13 were employed to differentiate monocyte into M2 macrophage. After 7 days of polarization, analysis of cell surface differentiation markers (CD86+/CD80+ for M1 and CD206+/CD200R+ for M2) and measurement of MerTK expression were performed using flow cytometry. Results Both M1 and M2 macrophage expressed similar level of CD86, CD80 and CD206 in all groups of CAD patients. MerTK expression in no apparent CAD patients was significantly higher in M2 macrophage compared to M1 macrophage [12.58 ± 4.40 vs. 6.58 ± 1.37, p = 0.040]. Conclusion Differential polarization of macrophage into M1 and M2 was highly dynamic and can be varied due to the microenvironment stimuli in atherosclerotic plaque. Besides, higher expression of MerTK in patients with the least coronary obstructive suggest its vital involvement in efferocytosis.

Background: Treatment of the left ventricular thrombus (LVT) with Vitamin K antagonists (VKAs) such as warfarin may lead to longer hospitalization. Thus, the potential of non-VKA oral anticoagulants as alternative to warfarin need to be explored. This study aims to investigate the size reduction or resolution of LVT with apixaban compared to conventional warfarin. Materials and Methods: This is a pilot, prospective, single-center, randomized, single-blinded outcome study with patients diagnosed with LVT. Patients diagnosed with LVT by echocardiography were randomized into two treatment groups: apixaban or warfarin, with target international normalized ratio 2–3. Echocardiography was repeated at weeks 6 and 12 to assess the LVT size. The percentage of reduction or total resolution during the first 12 weeks was the primary endpoint. Repeated measure ANCOVA was used to evaluate the differences in left ventricular (LV) thrombus size between treatment groups. Results: Twenty-seven patients were recruited: 14 were treated with apixaban and 13 patients with warfarin. Thirteen patients completed treatment in the apixaban arm with one patient lost to follow-up, and one death observed. In the warfarin arm, nine patients completed the study follow-up, and four died during the follow-up. The mean (standard deviation [SD]) reduction in LV thrombus size in apixaban arm was 65.1% (SD 31.3) versus warfarin arm, 61.5% (SD 44.0) at the 12th week follow-up (P = 0.816). Safety outcomes were similar with both treatment arms. Conclusions: This pilot study suggests that apixaban may have similar effectiveness and safety to warfarin for LVT resolution.

A reversed-phase HPLC method to determine total plasma warfarin was developed and validated. Warfarin was extracted from human plasma using a two-step liquid-liquid extraction method. The residue was reconstituted with a phenylbutazone standard solution, which was used as the internal standard. The analytical column was a Purospher STAR RP-18e (4 x 4mm I.D., 5m particle size). The mobile phase consisted of acetonitrile: potassium dihydrogen orthophosphate buffer solution at pH 6.5 [30:70 (v/v)] with a flow rate of 1mL/min. Both warfarin and phenylbutazone were detected using a photodiode array detector. The lower limit of quantification was 100ng/mL, while the limit of detection was 20ng/mL. The linearity of the assay was good (r2=0.992) in the concentration range from 0.1 - 6.0µg/mL. The extraction recovery of warfarin was 93.53 ± 12.40%. Both the intraday and interday quality control assay for warfarin demonstrated good precision and accuracy, with all of the percentage coefficients of variation being less than 15%. Warfarin was stable in human plasma for up to three months of storage. The validated method was successfully applied to four human samples for a pharmacokinetics study.

Background: Non-cardiac chest pain is common with two-thirds due to gastroesophageal reflux disease (GERD).Objective: To evaluate the effectiveness and safety of guided vs. empirical therapy in non-cardiac chest pain.Methods: Adults with normal angiogram or stress test were randomized into either a guided or empirical group. In the guided group, after the ambulatory pH-impedance test, if GERD then dexlansoprazole 30 mg/day for 8 weeks, but if functional or hypersensitive chest pain, then theophylline SR 250 mg/day for 4 weeks. In the empirical group, dexlansoprazole 60 mg/day was given for 2 weeks. The primary outcome was global chest pain visual analog score (VAS) and secondary outcomes were Quality of Life in Reflux and Dyspepsia (QOLRAD), GERD questionnaire (GERDQ), and pH parameters, all determined at baseline, 2nd and 8th weeks.Results: Of 200 screened patients, 132 were excluded, and of 68 randomized per-protocol, 33 were in the guided group and 35 in the empirical group. For between-group analysis, mean global pain scores were better with guided vs. empirical group at 8th week (P = 0.005) but not GERDQ or QOLRAD or any of pH measures (all P > 0.05). For within-group analysis, mean QOLRAD improved earliest at 8th week vs. baseline (P = 0.006) in the guided group and 2nd week vs. baseline (P = 0.011) in the empirical group but no differences were seen in other secondary outcomes (P > 0.05). No serious adverse events were reported.Conclusions: Guided approach may be preferred over short-term empirical therapy in symptom response, however QOLRAD, acid-related symptoms, or pH measures are not significantly different (trial registration ID no. NCT03319121).

Approximately half of all women presenting to the emergency department with angina chest pain do not have obstructive coronary artery disease (CAD) on coronary angiography. This condition is termed non-obstructive coronary artery disease (NOCAD), and includes ischemia with no obstructive coronary artery disease (INOCA) and myocardial infarction with non-obstructive coronary arteries (MINOCA). Oxidative stress has been reported to be involved in the development and progression of CAD. However, a scarcity of studies has assessed a correlation between oxidative stress and NOCAD. Thus, a literature review was performed of available reports on the role of oxidative stress in NOCAD. Possible mechanisms involved in oxidative stress that may contribute to NOCAD were identified and evaluated. A key finding of this literature review was that oxidative stress caused vasoconstriction and endothelial damage, and this results in coronary microvascular dysfunction and vasospasm, which, in turn, lead to the pathogenesis of NOCAD.