Yoichi Ajiro

Dabigatran for left atrial thrombus.

A 72-year-old woman was admitted to our hospital with acute exacerbation of chronic heart failure. Her medical history included chronic heart failure, permanent atrial fibrillation, and psychiatric disease. Despite a CHA2DS2-VASc score of 5, poor drug compliance compelled her to warfarin administration. Coarse crackles were evident over both lungs and a chest X-ray showed pulmonary congestion. Electrocardiography showed …

Platelet-activating factor stimulates sodium-hydrogen exchange in ventricular myocytes

Sodium-hydrogen exchanger (NHE), the principal sarcolemmal acid extruder in ventricular myocytes, is stimulated by a variety of autocrine/paracrine factors and contributes to myocardial injury and arrhythmias during ischemia-reperfusion. Platelet-activating factor (PAF; 1-o-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a potent proinflammatory phospholipid that is released in the heart in response to oxidative stress and promotes myocardial ischemia-reperfusion injury. PAF stimulates NHE in neutrophils and platelets, but its effect on cardiac NHE (NHE1) is unresolved. We utilized quiescent guinea pig ventricular myocytes bathed in bicarbonate-free solutions and epifluorescence to measure intracellular pH (pH(i)). Methylcarbamyl-PAF (C-PAF; 200 nM), a metabolically stable analog of PAF, significantly increased steady-state pH(i). The alkalosis was completely blocked by the NHE inhibitor, cariporide, and by sodium-free bathing solutions, indicating it was mediated by NHE activation. C-PAF also significantly increased the rate of acid extrusion induced by intracellular acidosis. The ability of C-PAF to increase steady-state pH(i) was completely blocked by the PAF receptor inhibitor WEB 2086 (10 μM), indicating the PAF receptor is required. A MEK inhibitor (PD98059; 25 μM) also completely blocked the rise in pH(i) induced by C-PAF, suggesting participation of the MAP kinase signaling cascade downstream of the PAF receptor. Inhibition of PKC with GF109203X (1 μM) and chelerythrine (2 μM) did not significantly affect the alkalosis induced by C-PAF. In summary, these results provide evidence that PAF stimulates cardiac NHE1, the effect occurs via the PAF receptor, and signal relay requires participation of the MAP kinase cascade.

Abrupt disruption of remote monitoring transmission as an indicator of safe backup mode

A 78-year-old man with sick sinus syndrome and accompanying persistent atrial tachyarrhythmia had undergone dual-chamber pacemaker (Evia DR-T™ Biotronik Inc., Germany) implantation with bipolar screw-in atrial and ventricular leads (Siello JT53™ and Siello S60™, Biotronik Inc.). Measured pacemaker and lead function values were within acceptable limits. Remote monitoring (Home Monitoring™ …

Contrast-Induced Nephropathy and Oxygen Pretreatment in Patients With Impaired Renal Function

Introduction Contrast-induced nephropathy is a complication following coronary angiography and percutaneous coronary intervention. Because contrast-induced nephropathy is a predictor of long-term mortality in patients with ischemic heart disease undergoing percutaneous coronary intervention, preventive strategies are required. We assessed the effects of periprocedural oxygenation on contrast-induced nephropathy among patients with pre-existing renal dysfunction. Methods A total of 200 consecutive patients with impaired renal function (estimated glomerular filtration < 60 ml/min per 1.73 m2) undergoing elective cardiovascular angiography were randomly assigned to an oxygenation treatment (n = 100) or control group (n = 100). In oxygenation treatment, pure oxygen (2 L/min) was administered for 10 minutes before exposure to contrast medium. The primary endpoint was the incidence of contrast-induced nephropathy, defined as a ≥ 25% increase in serum creatinine levels from baseline within 48 hours of exposure. Results In the oxygenation treatment group, partial pressure of arterial oxygen was higher (135 ± 25 mm Hg vs. 84 ± 10 mm Hg, P < 0.001); contrast-induced nephropathy incidence was lower (1% vs. 8%, odds ratio [OR] = 0.12, 95% confidence interval [CI] = 0.01–0.95, P = 0.02); and partial pressure of arterial carbon dioxide and bicarbonate base lactate levels were similar compared with those in the control group. Upon univariate analysis, excess and absence of oxygenation treatment (OR = 9.18, CI = 1.13–74.86, P = 0.03) and anemia (OR = 4.30, CI = 1.04–17.78, P = 0.04) were shown to be associated with contrast-induced nephropathy incidence. Conclusion Oxygenation, a simple, nonpharmacological strategy, may be beneficial when using contrast media in patients with impaired renal function from noninvasive angiography to emergency catheterization.

Surface electromyography of myopotential oversensing provoked by simultaneous straining and leftward twisting in a patient with an implantable cardioverter defibrillator

An important step in diagnosing myopotential oversensing is to confirm its reproducibility using specific provocation maneuvers. Although most maneuvers involve the co-contraction of many muscles, no attempt has been made to assess relevant muscle activities by electromyography. We describe a case with an implantable cardioverter defibrillator (ICD) whose myopotential oversensing was provoked by simultaneous straining and leftward twisting. Simultaneous recordings from real-time ICD telemetry and myopotentials of the rectus abdominis, oblique abdominis, and diaphragm on electromyography during the provocation maneuvers were conducted. It was shown that all three muscles contracted simultaneously during the provocation maneuvers; the diaphragm activity was the main source of noise oversensing, and the twist itself caused oversensing possibly due to the change in the position of the lead. In conclusion, the electromyographic assessment of relevant muscle activities may be useful in assessing each muscle’s role and its contribution to myopotential oversensing, especially in a patient whose myopotential oversensing requires complex maneuvers to be provoked.

Ventricular Fibrillation Due to Early Repolarization Syndrome in the Wake of Hypothermia Due to Fulminant Acute Disseminated Encephalomyelitis

(ADEM) was made based on elevated oligoclonal IgG bands, myelin basic protein level, and 80% monocytes in the CSF with absence of serum antibodies against commonly causal viruses. Magnetic resonance imaging (MRI) indicated extensive damage to the brainstem and cerebellum, A 44-year-old man was hospitalized for meningitis, with increased cell count and protein level in the cerebrospinal fluid (CSF). Despite treatment with antibiotics, he developed disturbed consciousness after 8 days. A diagnosis of acute disseminated encephalomyelitis

Myopotential oversensing notified by Lead Integrity Alert in a patient with implantable cardioverter defibrillator with a dedicated bipolar epicardial sensing lead

Although myopotential oversensing by a dedicated bipolar lead is rare, an epicardial lead on a dilated ventricle might contribute to its sensitivity. Myopotential oversensing was notified by the Lead Integrity Alert in this case. We should be aware of this possibility for the management of such patients.

Oxygen preconditioning prevents contrast-induced nephropathy in patients with chronic kidney disease: option CIN-CKD Randomized Trial

Purpose: Renal ischemia and direct toxicity of contrast media are involved in the pathogenesis of CIN. Our hypothesis was that sufficient oxygenation before contrast medium administration may mitigate kidney injury and reduce the incidence of CIN. The aim of this study was to assess the impact of oxygen preconditioning in preventing CIN for patients undergoing elective cardiovascular angiography. Methods: We studied 200 consecutive patients with chronic kidney disease (eGFR <60 mL/min/1.73 m2) undergoing elective cardiovascular angiography. Patients were selected and randomly assigned to either an oxygen preconditioning group (n = 100) or a control group (n = 100). Oxygen preconditioning was achieved by administering 2 L/min of pure oxygen 15 min before exposure to contrast medium. The primary endpoint was occurrence of CIN, defined as an increase in the serum creatinine levels of ≥ 25% or 0.5 mg/dL above the baseline level within 48 h of exposure. N-Acetyl-β-D-glucosaminidase (NAG) and the urinary liver-type fatty acid binding protein (L-FABP) were also evaluated at baseline and at the end of the procedure. The study was registered at UMIN-CTR with the identifier UMIN000007125. Results: In the oxygen preconditioning group, PaO2 was significantly higher (127±24 vs. 88±12 mmHg, P < 0.001) and the incidence of CIN was lower (2% vs. 11%, OR: 0.10, P = 0.01) compared to that of the control group. Multivariate analysis revealed that PaO2 <100 mmHg (OR 6.56, P = 0.02) was the only significant predictor of CIN. Oxygen preconditioning was associated with an 82% reduction in CIN incidence. (OR: 0.17, P < 0.001). Significantly greater reduction in NAG was observed in the oxygen preconditioning group than that in the control group (6.4±3.7 vs. 10.1±8.3 U/L, P < 0.05) at 2 days after the procedure. Conclusions: Oxygen preconditioning reduced the incidence of CIN in patients with reduced eGFR by reduction of the damage of renal proximal tube. This simple preventive strategy may be beneficial for patients with chronic kidney disease who undergo cardiac catheterization.