Essential thrombocythemia with non-ST-segment elevation myocardial infarction as the first manifestation: A case report.

BACKGROUND: We report a case of essential thrombocythemia (ET) in a 44-year-old male who exhibited non-ST-segment-elevation myocardial infarction (NSTEMI) as the first manifestation without known cardiovascular risk factors (CVRFs). For the first time, we reported a left main trifurcation lesion in NSTEMI caused by ET, including continuous stenosis lesions from the left main to the ostial left anterior descending (LAD) artery and an obvious thrombotic lesion in the ostial and proximal left circumflex (LCX) artery. There was 60% diffuse stenosis in the left main (LM) that extended to the ostial LAD, thrombosis of the ostial LAD and proximal LCX, and 90% stenosis in the proximal LCX. During the operation, thrombus aspiration was performed, but no obvious thrombus was aspirated. Performing the kissing balloon technique (KBT) in the LCX and LM unexpectedly increased the narrowness of the LAD. Then, the single-stent crossover technique, final kissing balloon technique and proximal optimization technique (POT) were performed. On the second day after percutaneous coronary intervention (PCI), the number of platelets (PLTs) still increased significantly to as high as 696 × 109/L. The bone marrow biopsy done later, together with JAK2 (exon 14) V617F mutation, confirms the diagnosis of ET. Hydroxyurea was administered to inhibit bone marrow proliferation to control the number of PLTs. CASE SUMMARY: A 44-year-old male patient went to a local hospital for treatment for intermittent chest pain occurring over 8 h. The examination at the local hospital revealed elevated cTnI and significantly elevated platelet. Then, he was diagnosed with acute myocardial infarction and transferred to our hospital for emergency interventional treatment by ambulance. During the operation, thrombus aspiration, the single-stent crossover technique, final kissing balloon technique and POT were performed. Dual antiplatelet therapy comprising aspirin and ticagrelor was used after PCI. Evidence of mutated JAK2 V617F and bone marrow biopsy shown the onset of ET. Together with JAK2 (exon 14) V617F mutation, ET was diagnosed according to the World Health Organization (WHO) diagnostic criteria, and the patient was placed on hydroxyurea. During the one-year postoperative period, repeated examinations showed a slight increase in PLTs, but the patient no longer had chest tightness, chest pain or bleeding or developed new thromboembolisms. CONCLUSION: Routine physical examinations and screenings are conducive to the early detection of ET, and the risk for thrombosis should be assessed. Then, active antiplatelet therapy and myelosuppression therapy should be used for high-risk ET patients.

Amelioration of ischemic cardiomyopathy in patients using physiological ischemic training.

BACKGROUND: This study aimed to observe the effect and potential mechanism of physiological ischemic training (PIT) in patients with ischemic cardiomyopathy. METHODS: A total of 165 patients with ischemic cardiomyopathy were randomly selected by the convenience sampling method and were divided into the control and experimental groups. The control group received conventional drug treatment, while the experimental group received additional PIT. All patients were followed up for 6 months and renin-angiotensin-aldosterone system (RAS) activity parameters and myocardial remodeling indicators were recorded. RESULTS: After the 6­month intervention, cardiac function indicators in the two groups were significantly improved compared with before intervention (all P < 0.01), but the experimental group showed significantly more improvement compared with the control group (all P < 0.01). Similarly, RAS activity parameters and myocardial remodeling indicators of the two groups were significantly reduced after intervention compared with before intervention (all P < 0.01). However, the experimental group showed significantly lower myocardial remodeling indicators than the control group (all P < 0.01). Vascular endothelial growth factor (VEGF) and nitric oxide (NO) concentrations in peripheral blood in the experimental group were significantly increased after intervention compared with before intervention (both P < 0.01). CONCLUSIONS: PIT can be applied in patients with ischemic cardiomyopathy on the basis of the original standardized drug treatment. PIT ameliorates cardiac blood flow reserve by increasing VEGF and NO concentrations in the peripheral blood, as well as by inhibiting the RAS system and myocardial remodeling. This ultimately improves the patient's cardiac function to a greater extent.

Effects of statin therapy on chronic kidney disease patients with coronary artery disease.

BACKGROUND: Long-term persistence of statin therapy provided an ongoing reduction in mortality among patients with and without a known history of CVD, and renoprotective effect on CKD patients. Until now, very few reports are available from China to address the effects of statin therapy in CKD + CAD patients. METHODS: We compared the effects of long-term statin therapy (follow-up time 4 years) in terms of cardiovascular events, all-cause death, and cardiac death among 254 CKD patients with or without CAD. RESULTS: Long-term statin therapy was much more effective in the CKD + CAD patients compared with CKD patients. In the CAD + CKD patients, long-term statins showed a 22.2% reduction in the CVs rate (P = 0.012). With regard to the all-cause and cardiac deaths, long-term statins had significant treatment effects on the CAD + CKD patients (reduction of about 28.1% in mortality rates, P < 0.001). In contrast, long-term statin therapy exerted no significant influence on the clinical outcomes of the CKD-only patients. CONCLUSION: Long-term statin therapy more dramatically reduced the CVs and mortality rates of the CKD patients with concomitant CAD. In contrast, CKD-only patients had a good prognosis and did not appear to require statin treatment.

Diosgenin glucoside protects against myocardial injury in diabetic mice by inhibiting RIP140 signaling.

Myocardial injury is often observed during diabetes, but the nature physiological association is unclear. Here, we investigated the protective effective of diosgenin glucoside (DG), a pharmacologically active saponin extracted from Tritulus terrestris L., against myocardial injury in type 2 diabetic (db/db) mice and its molecular mechanism of action. Levels of serum and myocardial tissues, blood glucose and inflammatory cytokines, as well as cardiac function indicators, of db/db mice were measured, and DG's mechanism of action was evaluated by immunohistochemistry and Western blotting. We found that long-term DG treatment improved glucose tolerance and lipid profiles, reduced production of IL-1ß, IL-6, and TNF-α, and decreased serum levels of the cardiac injury indicators creatine kinase and lactate dehydrogenase. Interestingly, DG also inhibited RIP140 signaling, which normally regulates transcription of estrogen receptor genes and influences expression of proinflammatory cytokines. Our study revealed a novel mechanism of DG's anti-inflammatory effect against myocardial injury via RIP140 signaling modulation in diabetic mice.