Pacemaker implantation for persistent sinus node dysfunction in a patient with COVID-19.

A 46-year-old woman was admitted with coronavirus disease-2019 infection. Symptomatic sinus bradycardia occurred, followed by congestive heart failure. Therapeutics such as isoproterenol, theophylline, and cilostazol could not safely improve her symptoms. She underwent pacemaker implantation 53 days after admission. Atrial pacing remained was at 60% after 6 months.

Diagnostic performance of calcification-suppressed coronary CT angiography using rapid kilovolt-switching dual-energy CT.

OBJECTIVES: Multi-detector-row computed tomography angiography (MDCTA) plays an important role in the assessment of patients with suspected coronary artery disease. However, MDCTA tends to overestimate stenosis in calcified coronary artery lesions. The aim of our study was to evaluate the diagnostic performance of calcification-suppressed material density (MD) images produced by using a single-detector single-source dual-energy computed tomography (ssDECT). METHODS: We enrolled 67 patients with suspected or known coronary artery disease who underwent ssDECT with rapid kilovolt-switching (80 and 140 kVp). Coronary artery stenosis was evaluated on the basis of MD images and virtual monochromatic (VM) images. The diagnostic performance of the two methods for detecting coronary artery disease was compared with that of invasive coronary angiography as a reference standard. RESULTS: We evaluated 239 calcified segments. In all the segments, the sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy for detecting significant stenosis were respectively 88%, 88%, 75%, 95% and 88% for the MD images, 91%, 71%, 56%, 95% and 77% for the VM images. PPV was significantly higher on the MD images than on the VM images (P < 0.0001). CONCLUSIONS: Calcification-suppressed MD images improved PPV and diagnostic performance for calcified coronary artery lesions. KEY POINTS: • Computed tomography angiography tends to overestimate stenosis in calcified coronary artery. • Dual-energy CT enables us to suppress calcification of coronary artery lesions. • Calcification-suppressed material density imaging reduces false-positive diagnosis of calcified lesion.

The evaluation of cardiac tamponade risk in patients with pericardial effusion detected by non-gated chest CT.

BACKGROUND: Although pericardial effusion is often identified using non-gated chest computed tomography (CT), findings predictive of cardiac tamponade have not been adequately established. PURPOSE: To determine the findings predictive of clinical cardiac tamponade in patients with moderate to large pericardial effusion using non-gated chest CT. MATERIAL AND METHODS: We performed a retrospective analysis of 134 patients with moderate to large pericardial effusion who were identified from among 4581 patients who underwent non-gated chest CT. Cardiac structural changes, including right ventricular outflow tract (RVOT), were qualitatively evaluated. The inferior vena cava ratio with hepatic (IVCupp) and renal portions (IVClow) and effusion size were measured. The diagnostic performance of each structural change was calculated, and multivariate analysis was used to determine the predictors of cardiac tamponade. RESULTS: Of the 134 patients (mean age, 70.3 years; 64 men), 37 (28%) had cardiac tamponade. The sensitivity and specificity were 76% and 74% for RVOT compression; 87% and 84% for an IVClow ratio ≥0.77; and 60% and 77% for an effusion size ≥25.5 mm, respectively. Multivariate logistic regression analysis demonstrated that RVOT compression, an IVClow ratio ≥0.77, and an effusion size ≥25.5 mm were independent predictors of cardiac tamponade. The combination of these three CT findings had a sensitivity, specificity, and accuracy of 81%, 95%, and 91%, respectively. CONCLUSION: In patients with moderate to large pericardial effusion, non-gated chest CT provides additional information for predicting cardiac tamponade.

Addition of losartan to angiotensin-converting enzyme inhibitors improves insulin resistance in patients with chronic heart failure treated without ß-blockers.

BACKGROUND: Angiotensin II and insulin resistance (IR) have clinical implications in the pathophysiology of chronic heart failure (CHF). However, it is still unclear whether the combination of an angiotensin-receptor blocker and angiotensin-converting enzyme inhibitor (ACEI) improves IR in CHF patients who do not receive ß-blockers. Thus, the aim of the present study was to evaluate the effects of losartan on glucose metabolism and inflammatory cytokines in CHF patients treated with ACEI but not ß-blockers. METHODS AND RESULTS: The effect of losartan treatment for 16 weeks on IR was analyzed in 16 CHF patients in a randomized crossover trial. Insulin level and homeostasis model IR index (HOMA-IR) decreased significantly (P<0.05), but fasting plasma glucose did not change significantly. Serum tumor necrosis factor (TNF)-α, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 levels were significantly decreased with losartan (P<0.05). Furthermore, the changes in IL-6 and MCP-1 levels were significantly correlated with the reduction in HOMA-IR (P<0.05), but the change in TNF-α levels was not significantly correlated. CONCLUSIONS: The addition of losartan to ACEI therapy improved IR and decreased inflammatory cytokines in CHF patients who did not receive ß-blockers.

Fenofibrate enhances neovascularization in a murine ischemic hindlimb model.

Fenofibrate have been illustrated to stimulate nitric oxide (NO) pathway, which plays pivotal roles in neovascularization. Here, we evaluated the effect of fenofibrate on neovascularization using a murine ischemic hindlimb model. C57BL/6J mice were treated with fenofibrate and/or NG-nitro-l-arginine methyl ester hydrochloride (l-NAME) for 28 days after ischemia operation. We exploited a concentration of L-NAME that did not affect blood pressure levels but suppress NO activity. Limb blood perfusion and capillary density in ischemic limb, serum NO levels, and aortic NOS activity were significantly increased by fenofibrate treatment when compared with the untreatment group. And, these effects were abolished by coadministration of L-NAME. Fenofibrate treatment significantly lowered serum triglyceride levels. Cotreatment of L-NAME did not inhibit serum triglyceride level, lowering effect of fenofibrate. These results suggested that the lowering in serum triglyceride levels is not involved in the improvement of neovascularization. In an in vitro experiment, fenofibrate stimulated NOS activity in human umbilical vein endothelial cells. Also, fenofibrate stimulated in vitro angiogenesis, and this effect was abolished by coincubation with L-NAME. In conclusions, fenofibrate enhanced neovascularization in a murine hindlimb ischemia model. The mechanism is most likely through activation of NO pathway in endothelial cells.

Status of uric acid management in hypertensive subjects.

Hyperuricemia in hypertensive subjects has been considered one of risk factors of cardiovascular diseases. We investigated the status of uric acid management in 799 hypertensive subjects (432 females and 367 males; mean age 70.9 years) managed by 43 doctors (19 cardiologists and 24 noncardiologists; 25 private practice doctors and 18 hospital doctors). The serum uric acid level was available in 85.7% of the patients. This availability was equivalent regardless of facility size, and more cardiologists than noncardiologists monitored this information. The prevalence of hyperuricemia was 17.5% and was higher in men and in patients with high triglyceridemia, left ventricular hypertrophy, renal dysfunction, proteinuria, and smokers, but was not higher in subjects with chronic heart failure, diabetes mellitus, and those with prescriptions for diuretics and beta-blockers. The average serum uric acid level was higher in men and patients with chronic heart failure, renal dysfunction, high triglyceridemia, low high-density cholesterolemia, smokers, and subjects prescribed beta-blockers. Fifty percent of hyperuricemic patients were medicated, and 48.6% of them cleared the uric acid target level (6 mg/dL). No differences were observed in the treatment rate or the achievement rate of the target between genders, concurrent diseases, and physician specialties. Although doctors, especially cardiologists, have a high concern for the serum uric acid level, they do not intervene intensively, and specific treatment for individual patterns is not routinely given. Thus, more attention to uric acid management is necessary in hypertensive subjects to prevent cardiovascular diseases.

Plasma levels of uridine correlate with blood pressure and indicators of myogenic purine degradation and insulin resistance in hypertensive patients.

BACKGROUND: The relationship between plasma uridine levels and blood pressure (BP), and indicators of muscular purine degradation and insulin resistance (IR) has been evaluated in hypertensive (HT) patients. METHODS AND RESULTS: In 36 HT patients and 10 normotensive subjects, seated BP was measured, and blood samples were drawn after overnight fast. In 18 of the HT patients, the semi-ischemic forearm test was performed to examine the release of hypoxanthine, ammonium and lactate. Plasma uridine levels were significantly higher than in the normotensive subjects. Fasting plasma insulin levels and homeostasis model assessment of IR correlated with plasma uridine levels in the HT patients. Plasma uridine levels showed a significant correlation with hypoxanthine, ammonia and lactate released from the semi-ischemic exercising muscles of the HT patients. CONCLUSIONS: Taken together with the positive correlation with indicators of IR, it is suggested that plasma uridine levels in HT are responsible for purine degradation and IR in skeletal muscles.

Small extra-adrenal pheochromocytoma causing severe hypertension in an elderly patient.

We report the case of a 67-year-old woman with severe hypertension caused by an extra-adrenal pheochromocytoma. The tumor was detected by 131I metaiodobenzylguanidine scintigraphy and it was found to be small (2 cm ø) by enhanced CT. After the extirpation of the tumor, the blood pressure of the patient immediately normalized. It should be taken into account that a small extra-adrenal pheochromocytoma can be one of the causes of secondary hypertension in elderly patients. Since small extra-adrenal pheochromocytomas are difficult to detect, it is also important to perform suitable examinations to establish the diagnosis. Furthermore, we emphasize the importance of an accurate diagnosis in elderly patients with pheochromocytoma, for they often have less symptomatology and more severe cardiovascular complications due to refractory hypertension than younger patients.

Allopurinol reduces neointimal hyperplasia in the carotid artery ligation model in spontaneously hypertensive rats.

Uric acid and oxidative stress promote cardiovascular diseases, including atherosclerosis and hypertension. Xanthine oxidase, through which uric acid is generated, is a free-radical generating enzyme. The aim of the current study was to investigate whether allopurinol, an inhibitor of xanthine oxidase activity, affects vascular remodeling and vascular smooth muscle cell (VSMC) proliferation. In the carotid artery ligation model using spontaneously hypertensive rats (SHR), treatment with allopurinol induced a reduction in the neointima/media ratio by 27% (38.5+/-34.3% in the control group and 28.1 20.8% in the allopurinol-treated group, respectively, p<0.01) without alterations in vascular circumference at 3 weeks after ligation when compared to the control. Allopurinol lowered the serum uric acid concentration (147.0+/-3.6 micromol/l in the control group and 16.1+/-3.6 micromol/l in the allopurinol-treated group, respectively p<0.01) and xanthine oxidase activity, but not the blood pressure. In an in vitro study, high concentrations of uric acid (100 and 200 micromol/l) stimulated VSMC growth, but there was no stimulation of these cells by a low concentration of uric acid (50 micromol/I) or by any of three concentrations of xanthine (50, 100 and 200 micromol/l). In addition, allopurinol (5 micromol/I) had no effect on the cell growth. In conclusion, uric acid is a potent stimulator of VSMC proliferation, and allopurinol prevented vascular remodeling in SHR at least in part by inhibiting uric acid concentration.

Inhibition of inward rectifier K+ currents by angiotensin II in rat atrial myocytes: lack of effects in cells from spontaneously hypertensive rats.

We examined the effects of angiotensin II (Ang II) on inward rectifier K+ currents (IK1) in rat atrial myocytes. [125I]Ang II-binding assays revealed the presence of both Ang II type 1 (AT1) and type 2 (AT2) receptors in atrial membrane preparations. Ang II inhibited IK1 in isolated atrial myocytes with an IC50 of 46 nmol/l. This inhibition was abolished by the AT, antagonist RNH6270 but not at all by the AT2 antagonist PD123319. Treatment of cells with pertussis toxin or a synthetic decapeptide corresponding to the carboxyl-terminus of Gialpha-3 abolished the inhibition by Ang II, indicating the role of a Gi-dependent signaling pathway. Accordingly, Ang II failed to inhibit IK1 in the presence of forskolin, dibutyryl-cAMP or protein kinase A catalytic subunits. In spite of the increased binding capacities for [125I]Ang II, Ang II failed to affect IKI in cells from spontaneously hypertensive rats (SHR). AT, immunoprecipitation from atrial extracts revealed decreased amounts of Gialpha-2 and Gialpha-3 proteins associated with this receptor in SHR as compared with controls. The reduced coupling of AT, with Gialpha. proteins may underlie the unresponsiveness of atrial IK1 to Ang II in SHR cells.