Digital zoom is a useful, simple, and cost-effective method of reducing radiation exposure in percutaneous coronary intervention.

Reducing radiation exposure is a very important issue in interventional cardiology techniques such as percutaneous coronary intervention. Although novel techniques to reduce radiation exposure are valuable, we should also reconsider older techniques. Digital zoom has been available in Japan from 2005. Digital zoom enlarges an 8-inch field of view (FOV) by 1.2 times, allowing visualization of a 6.7-inch FOV without FOV switching. We identified 2101 suitable cases of percutaneous intervention (PCI) and divided them into two groups according to the use of digital zoom; 1195 patients were included in the digital zoom group and 906 patients in the conventional group. We collected data regarding the reference air kerma (RAK) and dose-area product (DAP). We calculated RAK and DAP per minute fluoroscope time (RAK/min, DAP/min, respectively). There were intergroup differences in RAK, DAP, RAK/min, and DAP/min (digital zoom group vs conventional group; RAK, 1590 mGy [990-2410] vs 1850 [1220-2720], p < 0.01, RAK/min; 54.7 mGy/min [38.5-73.2] vs 71.2 [51.5-93.0], p < 0.01; DAP, 16,000 cGy × cm2 [10,300-24,400] vs 20,700 [13,400-29,500], p < 0.001; DAP/min, 557 cGy × cm2/min [392-737] vs 782 [571-1010], p < 0.01, respectively). Because of baseline differences between the two groups, we performed propensity score matching. Even after score matching, there were intergroup differences in DAP, DAP/min, RAK, and RAK/min. Furthermore, the least squares method showed that digital zoom is a significant predictor of RAK (ß = 0.14, p < 0.01) and DAP (ß = 0.20, p < 0.01). Digital zoom is an older cost-effective technique that can significantly reduce radiation exposure in PCI.

Correction to: The lactate clearance calculated using serum lactate level 6 h after is an important prognostic predictor after extracorporeal cardiopulmonary resuscitation: a single-center retrospective observational study.

[This corrects the article DOI: 10.1186/s40560-018-0302-z.].

Ultrasonographic and radiological imaging demonstrating an anomalous origin of the left coronary artery causing acute coronary syndrome in an adolescent.

We report the case of a 13-year-old girl who presented with cardiac collapse secondary to compression of the left main coronary artery (LMCA) between the pulmonary artery and the ascending aorta. In the acute phase, we performed aortography, intra-vascular ultrasound (IVUS), coronary computed tomography angiography (CCTA), transthoracic echocardiography (TTE), and transesophageal echocardiography (TEE). Aortography and CCTA showed that her LMCA was located between her pulmonary artery and the ascending aorta. IVUS and TEE showed that her LMCA was narrowed owing to compression by both great vessels during systole with release of the pressure during diastole. TTE and TEE showed that the left coronary artery flow was faster in the systole than that observed in the diastole. She was initially treated at our hospital but was transferred to another hospital for an unroofing operation. This was a rare case of a patient presenting with a coronary artery anomaly causing cardiac collapse. We conclude that her LMCA stenosis secondary to compression and narrowing of the great vessels led to her cardiac collapse. .

The lactate clearance calculated using serum lactate level 6 h after is an important prognostic predictor after extracorporeal cardiopulmonary resuscitation: a single-center retrospective observational study.

BACKGROUND: Serum lactate level can predict clinical outcomes in some critical cases. In the clinical setting, we noted that patients undergoing extracorporeal cardiopulmonary resuscitation (ECPR) and with poor serum lactate improvement often do not recover from cardiopulmonary arrest. Therefore, we investigated the association between lactate clearance and in-hospital mortality in cardiac arrest patients undergoing ECPR. METHODS: Serum lactate levels were measured on admission and every hour after starting ECPR. Lactate clearance [(lactate at first measurement - lactate 6 h after)/lactate at first measurement × 100] was calculated 6 h after first serum lactate measurement. All patients who underwent ECPR were registered retrospectively using opt-out in our outpatient's segment. RESULT: In this retrospective study, 64 cases were evaluated, and they were classified into two groups according to lactate clearance: high-clearance group, > 65%; low-clearance group, ≤ 65%. Surviving discharge rate of high-clearance group (12 cases, 63%) is significantly higher than that of low-clearance group (11 cases, 24%) (p < 0.01). Considering other confounders, lactate clearance was an independent predictor for in-hospital mortality (odds ratio, 7.10; 95% confidence interval, 1.71-29.5; p < 0.01). Both net reclassification improvement (0.64, p < 0.01) and integrated reclassification improvement (0.12, p < 0.01) show that adding lactate clearance on established risk factors improved the predictability of in-hospital mortality. CONCLUSION: In our study, lactate clearance calculated through arterial blood gas analysis 6 h after ECPR was one of the most important predictors of in-hospital mortality in patients treated with ECPR after cardiac arrest.

Prostacyclin synthase gene transfer modulates cyclooxygenase-2-derived prostanoid synthesis and inhibits neointimal formation in rat balloon-injured arteries.

Previous studies have shown that prostacyclin (PGI(2)) synthase (PCS) gene transfer inhibits neointimal formation in balloon-injured arteries. However, the role of each cyclooxygenase (COX) isoform in this healing mechanism remains unknown. We hypothesized that overexpression of PCS may modulate COX-2-mediated prostaglandin (PG) metabolism. That is to say, excessive PGH(2) derived from COX-2 after balloon injury may be converted into PGI(2) rather than PGE(2) or thromboxane (TX) A(2) by overexpressed PCS. We examined the expression of COX isoforms and evaluated the role of COX-2 with regard to the effects of PCS gene transfer by using 4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide (JTE-522), a selective COX-2 inhibitor. Rats were divided into 4 groups in conjunction with PCS gene transfer and JTE-522 treatment. The PCS gene (30 microg) was transfected into rat balloon-injured arteries by a lipotransfection method. JTE-522 (30 mg/kg per day) was administered for 14 days after balloon injury. Immunohistochemical analysis demonstrated marked COX-2 expression on the neointima. PCS gene transfer markedly inhibited neointimal formation, but JTE-522 reversed this beneficial effect. PCS gene transfer augmented PGI(2) production and decreased PGE(2) production without affecting TXA(2) production, but JTE-522 inhibited this increase in PGI(2) production. In conclusion, PCS gene transfer modulated COX-2-mediated prostanoid synthesis and inhibited neointimal formation after balloon injury.

Catheter-based prostacyclin synthase gene transfer prevents in-stent restenosis in rabbit atheromatous arteries.

OBJECTIVE: Prostacyclin synthase (PGIS) gene transfer have been shown to accelerate re-endothelialization and prevent neointimal formation in balloon-injured arteries. The aim of this study is to evaluate how overexpression of endogenous prostacyclin exerts those beneficial effects in atheromatous arteries. METHODS: New Zealand White Rabbits fed a 0.5% cholesterol diet underwent balloon injury and Palmaz-Schatz stent implantation in the iliac arteries followed PGIS gene (pCMV-PGIS, 200 microg) delivery by the lipotransfection method via Dispatch catheter (n=6 each). RESULTS: One week after transfection, arterial segments of pCMV-PGIS produced higher levels of 6-keto-PGF1alpha than those of control, pCMV-LacZ (p<0.05). The levels of vascular endothelial growth factor (VEGF) expression was greater in the vessels of pCMV-PGIS than in those of pCMV-LacZ demonstrated by immunohistochemical analysis and quantitation of Western blotting (1.8-fold, p<0.05). At 2 weeks, in-stent endothelialization was significantly greater in the vessels of pCMV-PGIS than in those of pCMV-LacZ (p<0.01). The percentage of BrdU-positive nuclei in the injured arterial segments was lower in vessels of pCMV-PGIS than pCMV-LacZ (p<0.01). At 4 weeks, PGIS gene transfer reduced the neointimal area by 38% (p<0.05) and widened the lumen area by 71% (p<0.01). CONCLUSION: PGIS gene transfer accelerated re-endothelialization, and attenuated neointimal formation after stent implantation in atheromatous rabbit arteries, at least in part, via increased production of VEGF protein.

Quinapril treatment restores the vasodilator action of insulin in fructose-hypertensive rats.

1. Angiotensin-converting enzyme (ACE) inhibitors have been shown to improve insulin-resistance both experimentally and clinically. We therefore investigated the effects of quinapril, which has high tissue specificity for ACE, regarding the contribution of insulin to vascular contractions, as well as insulin sensitivity in a dietary rat model of insulin resistance. 2. Male Sprague-Dawley rats were divided into three groups: (i) rats fed normal chow (normal diet group); (ii) rats fed fructose-rich chow containing 40% fructose and 7% lard (fructose diet group); and (iii) rats fed fructose-rich chow plus quinapril (10 mg/kg per day; quinapril-treated group). 3. After 2 weeks, we evaluated systolic blood pressure, insulin sensitivity as assessed by steady state plasma glucose (SSPG) levels, response of aortic rings to phenylephrine (10-9 to 10-6 mol/L) in the presence or absence of insulin and the response of aortic rings to acetylcholine. 4. Feeding rats fructose-rich chow resulted in an elevation of blood pressure (P < 0.01) and SSPG levels (P < 0.01). Quinapril treatment significantly prevented increases in both blood pressure and SSPG, with a return to the levels seen in the normal diet group. 5. In the absence of insulin, the maximal contractile response to phenylephrine did not differ between the three groups. However, in the presence of insulin (100 mU/mL), the contractile response to phenylephrine (10-6 mol/L) was reduced by 22.8 +/- 1.2% in the normal diet group, although no insulin effects were observed in the fructose diet group (P < 0.01). Quinapril restored the inhibitory effect of insulin on phenylephrine-induced contractions. 6. In addition, the reduction in relaxation induced by acetylcholine in the fructose diet group was significantly reversed by quinapril treatment. 7. It is concluded that the fructose diet impairs the vasodilator effects of insulin as well as acetylcholine-induced relaxation in rat thoracic aortas. Quinapril prevented deterioration in the responses of the aortic rings, suggesting that ACE inhibitors may be useful for treating vascular insulin resistance.