Coronary artery calcification scoring system based on the coronary artery calcium data and reporting system (CAC-DRS) predicts major adverse cardiovascular events or all-cause death in patients with potentially curable lung cancer without a history of cardiovascular disease.

The coronary artery calcium data and reporting system (CAC-DRS) is a novel reporting system based on CAC severity. Lung cancer patients have a high risk of cardiovascular disease (CVD), for which CAC severity may provide additional prognostic information. Using non-gated, non-contrast computed tomography (CT), we evaluated the CAC-DRS for predicting CVD and all-cause death in patients with potentially curable resected lung cancer. We retrospectively studied 309 consecutive patients without a history of CVD (mean age 67.4 ± 8.2 years, 61% male) who underwent curative surgery for non-small-cell lung cancer between May 2012 and March 2019 at the Japanese Red Cross Okayama Hospital. Time to incidence of major adverse cardiac events (MACEs) (non-fatal myocardial infarction, non-fatal stroke and cardiovascular death) and all-cause death was analyzed using Fine and Gray and Cox regression models. The CAC-DRS score was assessed using standard chest CT without electrocardiogram gating. During 52-months' median follow-up, 43 patients (13.4%) developed incident MACEs or died from any cause; the pathological cancer stages were Ia (n = 20), Ib (n = 8), IIa (n = 2), IIb (n = 2) and IIIa (n = 11). Patients had a graded increase in incidence of MACEs or all-cause death with increasing categories of CAC-DRS. The CAC-DRS score was significantly associated with incident MACEs or all-cause death after adjusting for confounding factors (hazard ratio 1.18; 95% confidence interval 1.10-1.25, p < 0.01). In conclusion, the CAC-DRS score on non-gated standard CT can predict incident MACEs and/or all-cause death in patients with potentially curable resected lung cancer. Lung cancer survivors with a greater CAC-DRS category may need more active management of cardiovascular risk factors.

Diagnostic Accuracy of Three Different Protocols for 3.0T Coronary Magnetic Resonance Angiography.

The usefulness of coronary magnetic resonance angiography (cMRA) has been reported, although the difference in the diagnostic accuracy of different protocols has not been established.We compared conventional coronary angiography (CAG) and cMRA, conducted within 6 months in 24 consecutive patients between September 2012 and July 2014. Three cMRA protocols were examined, cMRA1, free-breathing wholeheart coronary angiography (WHCA) without contrast; cMRA2, free-breathing WHCA with contrast; and cMRA3, breath-hold steady-state free precession with contrast using a 3.0 T scanner. Image quality was graded on a 4-point scale: 1) nonassessable; 2) assessable, fair vessel contrast; 3) assessable, good vessel contrast; and 4) assessable, excellent vessel contrast. Significant narrowing of the coronary arteries was visually assessed.Stenosis was observed in 34 segments, with a prevalence of 10.3%. For cMRA1, cMRA2, and cMRA3, the numbers of assessable segments were 245 (74.2%), 287 (87.0%), and 164 (49.7%), respectively (P < 0.001 by the McNemar test). For assessable segments, the sensitivity, specificity, positive predictive value, and negative predictive value were 89.3%, 99.1%, 92.6%, and 98.6% for cMRA1, 90.0%, 98.1%, 84.4%, and 98.8% for cMRA2, and 76.5%, 93.9%, 59.1%, and 97.1% for cMRA3, respectively. For the assessable segments, the image quality score was better with cMRA2 than with the other two protocols.cMRA is a useful modality to rule out coronary artery disease, especially the cMRA2 protocol, which performed better than the other two protocols.

Double congenital fistulae with aneurysm diagnosed by combining imaging modalities.

Congenital coronary pulmonary artery fistula (CAF) is rare, and systemic-to-pulmonary artery fistula (SPAF) is even more so. Furthermore, congenital coronary pulmonary fistula associated with congenital SPAF is extremely rare. As far as we know, CAF and SPAF connected with an aneurysm have not been described very often. We described an 83-year-old woman with an aneurysm originating from a CAF connected to an aortopulmonary artery fistula. Chest radiography revealed a shadow at the left edge of the heart line. Multi-detector-row computed tomography (MDCT) with contrast enhancement and coronary cine angiography revealed that the shadow was an aneurysm connected to a tortuous fistula at the left anterior descending coronary artery. The aneurysm was formed by congenital coronary pulmonary and aortopulmonary artery fistulae. Echocardiography revealed predominantly systolic blood flow in the fistula from the left anterior descending coronary artery (LAD). Although neither MDCT, echocardiography nor coronary angiography alone could provide a comprehensive image of the anomaly, including the hemodynamics in the fistulae and their relationship with surrounding organs and tissues, their combination could provided important facts the led to a deeper understanding of this very uncommon occurrence.

Detrended fluctuation analysis can detect the impairment of heart rate regulation in patients with heart failure with preserved ejection fraction.

BACKGROUND: The impairment of short-term heart rate regulation in patients with heart failure with preserved ejection fraction (HFpEF) can cause acute hemodynamic collapse. Detrended fluctuation analysis (DFA) is a useful tool for the diagnosis of heart diseases and the prediction of mortality. In DFA, the short-term scaling exponent α is decreased in heart failure. However, its change in HFpEF patients remains unclear. METHODS: Twenty patients diagnosed with HFpEF [defined as brain natriuretic peptide (BNP) >100 pg/mL, ejection fraction (EF) ≥50%, and without significant valvular disease], 20 diagnosed with non-HFpEF (BNP > 100 pg/mL and EF < 50%), and 20 control subjects generally matched for age and gender were enrolled. Holter electrocardiography was performed, and heart rate variability was calculated. In the DFA, the scaling exponents in 1000 beats were calculated for each 15-min segment and the average of all segments was used. We compared both the short-term (<11 beats, α1) and long-term (≥11 beats, α2) scaling exponents among the three groups. RESULTS: In the HFpEF, non-HFpEF, and control groups, α1 was 0.73 ± 0.27, 0.66 ± 0.29, and 1.01 ± 0.20 (p < 0.01), and α2 was 0.95 ± 0.08, 0.88 ± 0.11, and 0.96 ± 0.07 (p < 0.01), respectively. The α1 exponent was significantly decreased in the HFpEF group (p < 0.01 vs. control) and the non-HFpEF group (p < 0.01 vs. control), while the α2 exponent was significantly decreased in the non-HFpEF group only (p < 0.05 vs. HFpEF and control). CONCLUSIONS: Short-term heart rate regulation is impaired in patients with HFpEF, while patients with non-HFpEF have both short-term and long-term impairment.

Postprandial hypotension due to a lack of sympathetic compensation in patients with diabetes mellitus.

Postprandial hypotension is an important hemodynamic abnormality in diabetes mellitus, but few reports are available on the relationship between autonomic dysfunction and postprandial hypotension. Ten diabetic patients and 10 healthy volunteers were recruited for this study. Postural blood pressure and heart rate changes were measured before lunch, and then the hemodynamic responses to a standardized meal were investigated. Holter electrocardiogram (ECG) monitoring was conducted for assessing spectral powers and time-domain parameters of RR variations. Postural changes from the supine to the upright position decreased the systolic blood pressure of the diabetics from 133(+/-)16 to 107(+/-)20 mmHg (p<0.01), but did not decrease the systolic blood pressure of the controls. The heart rate remained constant in the diabetics but was increased in the controls. Food ingestion decreased systolic blood pressure in the diabetics, with a maximum reduction of 25(+/-)5 mmHg. This decrease was not associated with any changes in the ratio of low frequency to high frequency, and yet the heart rate remained almost constant. Indexes involving parasympathetic tone were not affected. Food ingestion did not affect blood pressure in the control group. These findings suggest that lack of compensatory sympathetic activation is a factor contributing to postprandial hypotension in diabetics, and that parasympathetic drive does not make a significant contribution to this condition.

Clinical significance of platelet reactivity during prasugrel therapy in patients with acute myocardial infarction.

BACKGROUND: Although some studies have examined platelet reactivity (PR) during prasugrel treatment, little is known about PR during the early treatment period and its clinical significance in Japan. METHODS: We investigated the early and medium-term efficacy and safety of prasugrel in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI). Seventy-eight patients were enrolled and PR was measured (in P2Y12 reaction units; PRU) by the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA, USA). RESULTS: In 44 patients, serial measurement revealed that PR was significantly higher at 2h after administration of the 20-mg loading dose of prasugrel than on the morning of the second day at 17.6±6.6h after administration (191.6±75.5 vs. 138.5±68.9PRU). During the 8-month follow-up period, bleeding events occurred in 18 patients (23.1%) (GUSTO minor: 15 patients). Multivariate regression analysis identified oral anticoagulant use as a significant predictor of bleeding events during admission [odds ratio (OR): 4.214, 95% confidence interval (CI): 1.005-17.669, p=0.049]. Administration of prasugrel via a nasogastric tube was a significant predictor of high on-treatment platelet reactivity (HTPR) (PRU≥230) (OR: 43.100, 95% CI: 4.517-411.251, p=0.001). In addition, HTPR was a significant predictor of major adverse cardiac events (cardiovascular death, non-fatal myocardial infarction, stent thrombosis, stroke, and sustained ventricular tachycardia) during the 8-month follow-up period (OR: 4.911, 95% CI: 1.164-20.722, p=0.030). CONCLUSIONS: It is feasible to treat AMI patients with prasugrel. HTPR is a significant independent risk factor for adverse events in AMI patients receiving prasugrel after primary PCI.

Hepatocyte growth factor gene therapy reduces ventricular arrhythmia in animal models of myocardial ischemia.

It was recently reported that gene therapy using hepatocyte growth factor (HGF) has the potential to preserve cardiac function after myocardial ischemia. We speculated that this HGF gene therapy could also prevent ventricular arrhythmia. To investigate this possibility, we examined the antiarrhythmic effect of HGF gene therapy in rat acute and old myocardial infarction models. Myocardial ischemia was induced by ligation of the left descending coronary artery. Hemagglutinating virus of Japan (HVJ)-coated liposome containing HGF genes were injected directly into the myocardium fourteen days before programmed pacing. Ventricular fibrillation (VF)was induced by programmed pacing. The VF duration was reduced and the VF threshold increased after HGF gene therapy ( p< 0.01). Histological analyses revealed that the number of vessels in the ischemic border zone was greatly increased after HGF gene injection. These findings revealed that HGF gene therapy has an anti-arrhythmic effect after myocardial ischemia.

Ultrasonography is convenient and useful for assessment and follow-up of Takayasu's arteritis.

A 20-year-old woman first came to our hospital complaining of high fever and pain affecting the whole body. Takayasu's arteritis (TA) was diagnosed. Following full-body examination, many vessels between the bilateral neck and iliac arteries were found to be impaired. Ultrasonography (US) showed the characteristic wall thickening of TA in the left common carotid artery. After starting prednisolone treatment (40 mg/day), symptoms improved quickly and vessel walls gradually became thinner. However, chest pain recurred when prednisolone was tapered to 20 mg/day. Blood tests showed no signs of recurring inflammation, and US revealed worsened wall thickening only in the left carotid artery. We therefore diagnosed local recurrence of activation of TA. Assessing local recurrence of TA with a blood test is difficult, particularly after prescribing steroids. In this case, US identified the local changes attributable to TA before any other diagnostic modality. US can be useful in assessing inflammation and offers a good strategic tool for initial diagnosis of TA.