Survival rate in patients with stage D heart failure has improved significantly owing to the development of continuous flow left ventricular assist devices (LVAD), but aortic insufficiency (AI) still remains one of the major unsolved complications that impairs patient quality of life. There are no established treatments for AI, and preoperative prediction and prevention of AI is needed. The opening of a native aortic valve (AV) is a sufficient condition for prevention of AI, and improvement of LV ejection fraction due to LV reverse remodeling (LVRR) is essential to open a native AV. Preoperative insufficient β-blocker treatment and pulsatile flow LVAD usage are keys for LVRR, opening of an AV, and prevention of AI. The second mechanism that leads to AI is remodeling of the aortic root and degeneration of a native AV, which results from reduced pulse pressure during LVAD support. Centrifugal or pulsatile flow LVAD usage has an advantage in terms of preserving pulsatility, and may prevent AI compared with an axial pump. There is less probability of avoiding AI with sufficient β-blocker treatment, and these patients may be good candidates for concomitant surgical intervention to a native AV at the time of LVAD implantation.
Inflammatory biomarkers have been proposed for use in the risk stratification of patients with acute myocardial infarction (AMI). We examined the value of inflammatory biomarkers over clinical features for predicting cardiovascular (CV) events in stable outpatients with MI. We enrolled 430 post-MI patients and measured their levels of high-sensitivity C reactive protein (hs-CRP), growth differentiation factor-15 (GDF-15), and the interleukin-1 receptor family member called ST2 (ST2), one month after AMI. Patients were prospectively followed for 3 years. In our study cohort (mean age, 66 ± 12 years; left ventricular ejection fraction, 55 ± 13%), CV events were observed in 39 patients (9.1%). Kaplan– Meier analysis revealed that patients with high levels of GDF-15 (≥ 1221.0 ng/L) showed poorer prognoses than those with low levels of GDF-15 (< 1221.0 ng/L) (20.4% versus 3.6%, P < 0.001); hs-CRP and ST2 did not show a similar correlation with prognoses. GDF-15 remained associated with CV events after adjusting for age, chronic kidney disease, and B-type natriuretic peptide (hazard ratio, 1.001; 95% confidence interval, 1.000 – 1.001; P = 0.046). GDF-15 provided an incremental predictive value for CV events over clinical features (incremental value in global χ2 = 43.81, P < 0.001). In outpatients with prior MI, GDF-15 was an independent indicator of CV events, unlike hs-CRP and ST2. GDF15 provided an incremental prognostic value over clinical features.
The role of pentraxin 3 (PTX3) has been implicated in the process of plaque vulnerability. However, few studies have addressed the direct relationship between plaque morphology and plasma PTX3. We evaluated the relationship between coronary vulnerable plaque, assessed by optical coherence tomography (OCT), and plasma PTX3 in patients with coronary artery disease (CAD). OCT was used to determine plaque vulnerability in 51 patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS; n = 17) and stable angina (SA; n = 34). Both highly-sensitive C-reactive protein and systemic plasma PTX3 were measured. Based on the OCT findings, patients were divided into 3 groups; a fibrous plaque (n = 18), thick-cap fibroatheroma (ThCFA) (n = 19), and thin-cap fibroatheroma (TCFA) (n = 14) groups. ThCFA was defined as a lipid-rich plaque (lipid content in ≥ 2 quadrant) covered with ≥ 65 μm thick fibrous cap, and TCFA was that with < 65 μm. There were no differences in patient characteristics between the 3 groups except for the presence of ACS and eicosapentaenoic acid levels. TCFA was more frequently observed with plaque rupture and intraluminal thrombus compared with the other 2 groups. Plasma PTX3 levels were higher in the TCFA group compared with the fibrous plaque and ThCFA groups, and showed weak correlation with cap thickness. Plasma PTX3 level was associated with plaque vulnerability assessed by OCT in patients with CAD.
Dormant pulmonary vein (PV) conduction revealed by adenosine/adenosine triphosphate (ATP) provocation test and exit block to the left atrium by pacing from the PV side of the ablation line (“pace and ablate” method) are used to ensure durable pulmonary vein isolation (PVI). However, the mechanistic relation between ATP-provoked PV reconnection and the unexcitable gap along the ablation line is unclear. Forty-five patients with atrial fibrillation (AF) (paroxysmal: 31 patients, persistent: 14 patients; age: 61.1 ± 9.7 years) underwent extensive encircling PVI (EEPVI, 179 PVs). After completion of EEPVI, an ATP provocation test (30 mg, bolus injection) and unipolar pacing (output, 10 mA; pulse width, 2 ms) were performed along the previous EEPVI ablation line to identify excitable gaps. Dormant conduction was revealed in 29 (34 sites) of 179 PVs (16.2%) after EEP-VI (22/45 patients). Pace capture was revealed in 59 (89 sites) of 179 PVs (33.0%) after EEPVI (39/45 patients), and overlapping sites, ie, sites showing both dormant conduction and pace capture, were observed in 22 of 179 (12.3%) PVs (17/45 patients). Some of the ATP-provoked dormant PV reconnection sites were identical to the sites with excitable gaps revealed by pace capture, but most of the PV sites were differently distributed, suggesting that the main underling mechanism differs between these two forms of reconnection. These findings also suggest that performance of the ATP provocation test followed by the “pace and ablate” method can reduce the occurrence of chronic PV reconnections.
Although oral amiodarone (AMD) has been used for the management of atrial fibrillation (AF), serious complications such as interstitial pneumonia (IP) occur very occasionally. We evaluated which factors were associated with the development of IP under the long-term administration of AMD in patients with refractory AF. This study included 122 consecutive patients (65.8 ± 11.4 years, mean body mass index [BMI] of 23.2 ± 4.3 kg/m2) who orally received AMD to inhibit AF between January 2004 and December 2013. Administration of AMD was begun at 400 mg daily as a loading dose, and was continued at a dosage of 50-400 mg daily after the initial loading phase, determined by the control of the arrhythmias and occurrence of side-effects. The clinical factors were compared between the patients with and without adverse effects, especially IP. During an average follow-up period of 49.2 ± 28.2 months, 53 patients (43.4%) were determined to have converted and maintained sinus rhythm. In contrast, adverse effects were detected in 46 patients (37.7%) with AMD. IP occurred in 8 patients (6.6%), thyrotoxicosis in 35 (28.7%), and others in 5 (4.1%). Four (50.0%) out of 8 patients complicated with IP had obesity (BMI > 27 kg/m2). Among the clinical factors, only obesity was significantly associated with the development of IP (P = 0.026). In patients with refractory AF, AMD had an antiarrhythmic effect with long-term administration, but greater adverse effects were also observed. Obesity was the most significant factor associated with the development of IP.
There are differences in reporting bleeding complications after transcatheter aortic valve implantation (TAVI), which is a consequence of the lack of consensus for their definition. Furthermore, the amount of data on the impact of peri-procedural bleeding on the mid-term prognosis is still limited. The aim of this study was to investigate the incidence, predictors, and impact of life-threatening and major bleedings as defined by the Valve Academic Research Consortium 2 (VARC-2) in patients after TAVI over the mid-term prognosis. Consecutive patients who underwent TAVI from March 2010 to December 2013 were included. All data were classified according to the VARC-2 criteria. We assessed the incidence and the predictors of serious bleeding events (SBE), defined as life-threatening/disabling (LT/D) or major bleeding, and analyzed their impact on 30-day and 1-year clinical outcome. A total of 129 patients were included (79.1 ± 8.3 years; mean EuroSCORE = 17.8 ± 12.7). The SBE occurred in 25 patients (19.4%), of which 9 (7.0%) had LT/D and 16 (12.4%) had major bleeding. Trans-subclavian (TS) access (OR 4.38, 95% CI 2.13–14.29, P = 0.01) and diabetes (OR 2.93, 95% CI 1.08–7.93, P = 0.03) were identified as independent predictors of SBE. Patients with SBE had higher 30-day mortality (20.0% versus 4.0% P = 0.02) and 1-year mortality (40.0% versus 11.1%, P < 0.002). SBE independently predicted 1-year, all-cause mortality (HR 5.88, 95% CI 1.7319,94, P = 0.005). SBE are frequent after TAVI and are associated with decreased short and mid-term survival. Diabetes and TS access are independent risk factors for SBE.
The urine aquaporin-2 (U-AQP2) level relative to the plasma arginine vasopressin (P-AVP) level is a novel predictor of the responsiveness to the vasopressin type 2 receptor (V2R) antagonist tolvaptan (TLV). However, little has been reported about the concentration-time profile of U-AQP2 after TLV treatment. We evaluated 24 patients with decompensated stage D heart failure (HF) who had received 3.75 mg/day of TLV on a de novo basis for > 7 days to treat congestion refractory to conventional diuretics. Seventeen patients were TLV-responders, whose 24-hour urine volume (UV) increased after TLV initiation; the other 7 patients were TLV-non-responders. The U-AQP2 of the TLV-responders, corrected for the urine creatinine concentration, decreased significantly at 4 hours after TLV administration without returning to the day-1 morning level on the morning of day-7. The TLV-non-responder U-AQP2 levels remained low even before the TLV treatment. On the morning of day-7, the TLV-responder U-AQP2/P-AVP ratio was comparable to that of the TLV-non-responders. Among 18 patients (11 responders and 7 non-responders), the day-7 TLV trough concentration was 64 ± 62 ng/mL and was negatively correlated with the estimated glomerular filtration rate (eGFR). TLV has antagonistic effects on the V2R over 24 hours in TLV-responders with advanced heart failure and chronic kidney disease, probably due to persistently elevated blood TLV concentration. The unresponsiveness to TLV in the TLV-non-responders is not attributable to malabsorption.
Adaptive servo-ventilation (ASV) is a recently developed, noninvasive therapeutic tool for the treatment of heart failure (HF). However, the efficacy of ASV therapy in patients with advanced HF remains uncertain, especially as regards its contribution to freedom from cardiac replacement therapy. A total of 85 patients with advanced HF (New York Heart Association [NYHA] class IV 71%, inotrope infusion-dependent 34%) refractory to guideline-directed medical therapy, received ASV therapy, irrespective of sleep-disordered breathing, at our institute between 2008 and 2014. Among these 85 patients, 46 continued ASV therapy for > 1 month (continued group), whereas 39 discontinued the therapy after < 1 month because of intolerance (discontinued group). There were no significant differences in baseline variables between the two groups. Heart rate indicating sympathetic activity, left ventricular (LV) reverse remodeling assessed by LV diastolic diameter, LV ejection fraction, and the grades of mitral and tricuspid regurgitations, HF severity assessed by NYHA class and plasma level of B-type natriuretic peptide, and end-organ dysfunction, improved significantly at 6 months following the initiation of ASV therapy (P < 0.05 for all). All-cause mortality and cardiac death rate were significantly lower during 2-year follow up in the continued group (P < 0.05 for both). In conclusion, ASV is a novel therapeutic tool prior to cardiac replacement therapy in patients with advanced HF and may prolong the period until cardiac replacement therapy becomes necessary.
Although calcium channel blockers (CCB) are expected to improve the augmentation index (AI) in CKD patients, the potential effect of benidipine on AI has been poorly studied. The present study aimed to compare the effect of benidipine and amlodipine in the treatment of CKD patients as measured through AI and urinary albumin excretion (UAE). Eligible patients with CKD were randomized to either the benidipine group or amlodipine group. Changes in UAE and AI were compared with target blood pressure level set at < 130/80 mmHg. A total of 108 patients were enrolled; 88 patients who were followed up were included in the analysis. Although no significant change in renal function was noted in either group, there was a significant improvement in AI only in the benidipine group (85.7 ± 13.3% to 81.4 ± 15.2%; P = 0.021) A subgroup analysis of 64 patients who achieved SBP < 140 mmHg at the end of follow-up (31 on amlodipine and 33 on benidipine) was carried out. Significant improvement in AI was noted only in the benidipine group (84.5 ± 13.6% to 79.5 ± 15.2%; P = 0.0138). In another subgroup of patients with UAE ≥ 300 mg/g Cr, a significant improvement in UAE in the benidipine group was found compared with the amlodipine group (-25 ± 46, 51 ± 60%, P = 0.031, respectively). These results suggest that benidipine might reduce significantly AI and might have potentially greater improvements in UAE than amlodipine in advanced CKD patients receiving RAS inhibitors.
There have been very few studies on serum biomarkers associated with hypertension in disaster situations. We assessed biomarkers associated with disaster-related hypertension (DRH) due to the Great East Japan Earthquake of March 2011. We collected blood samples from members of the Japan Self Defense Forces (JSDF) (n = 77) after completing disaster relief operations. We divided them into two groups based on systolic blood pressure. We defined DRH as either systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg at the time of completing missions. In subjects with DRH, the mean blood pressure was 143.5 ± 5.0/99.5 ± 2.4 mmHg. Height and body weight measurements were slightly greater in the DRH group but the differences were not significant, and age was significantly higher in the DRH group. There were no differences in serum biochemical tests including metabolic markers, sulfur-containing amino acids, and cytokines. Among nitric oxide-related amino acids, asymmetric dimethylarginine (ADMA) was lower in the DRH group than in the normotension group (0.40 ± 0.02 versus 0.31 ± 0.02 μmol/L P = 0.04). The serum oxidative stress metabolite levels (d-ROMs; indicators of active oxygen metabolite products) were significantly higher in the DRH group (273.6 ± 6.08 versus 313.5 ± 13.7 U.CARR P = 0.016). Using multivariable regression analysis, d-ROMs levels were particularly predictive for DRH. Oxidative stress is associated with DRH in responders to the disaster of the Great East Japan Earthquake.
Patients admitted to an intensive cardiac care unit (ICCU) are a heterogeneous population with a high mortality rate. The aim of our study was to investigate which clinical, biochemical, and echocardiographic parameters routinely assessed may affect long-term mortality in a non-selected ICCU population. A total of 392 patients hospitalized between 2008-2011 (mean age, 70 ± 13.8 years, 43% women) were consecutively and prospectively assessed with the following admission diagnoses: 168 with acute coronary syndromes (ACS), 122 with acute decompensated heart failure (ADHF), and 102 with other acute cardiac disorders. Patients were treated according to the current European Society of Cardiology (ESC) guidelines. During a mean 29.3 (± 18.9) months of observation, 152 (38.8%) patients died and 7.9% of the patients needed a red blood cell transfusion (RBC Tx). Patients who died were significantly older and had lower baseline levels of hemoglobin (Hb), serum iron concentration (SIC), total iron binding capacity (TIBC), cholesterol, and left ventricular ejection fraction (LVEF), as well as lower eGFR values, and higher white blood cell (WBC) counts and C-reactive protein (CRP) levels (P < 0.05). Predictors of death in multivariate regression analysis were age, Hb, LVEF, WBC, and CRP. The most powerful factor was hospitalization for non-ACS. The risk of long-term mortality increased with decreasing levels of Hb (P < 0.001), SIC (P = 0.001), TIBC (P = 0.009), and the need for RBC Tx (P < 0.001), as well as the diagnosis of ADHF (P < 0.001) and the absence of ACS (P = 0.007). In ICCU patients, age, Hb, parameters of iron status, and LVEF are strong predictors of long-term mortality. Among the ICCU population, patients with ACS diagnosis have better survival.
Arterial stiffness is associated with atherosclerosis and left ventricular (LV) diastolic function in general or hypertensive patients. However, the relationships between the arterial stiffness index measured at the radial artery and LV diastolic dysfunction in asymptomatic high-risk patients without atherosclerotic cardiovascular disease (ASCVD) have not been fully established. A total 532 statin-naïve patients (male:female ratio, 230:302, mean age, 56.0 ± 9.2 years) without ASCVD were enrolled from among subjects who simultaneously underwent transthoracic echocardiography and noninvasive semiautomated radial artery applanation tonometry from July 2011 to May 2014. Of these patients, 213 were categorized as the statin benefit group (Benefit) according to guidelines for blood cholesterol treatment, and the rest were placed in the nonbenefit control group (NoBenefit). Each group was subdivided into two groups (Y or N) according to antihypertensive medication administration. Thus, there were 4 groups: BenefitN (n = 80), BenefitY (n = 133), NoBenefitN (n = 251), and NoBenefitY (n = 68). There were significant differences in echocardiographic parameters of LV function and indices of arterial stiffness between the Benefit and NoBenefit groups. After adjusting for several risk factors, independent significant associations between echocardiographic parameters of LV diastolic function and arterial indices were identified with multivariate linear regression analysis in the Benefit patients. Parameters of arterial stiffness measured at the radial artery are associated with echocardiographic indices of LV diastolic function in asymptomatic high-risk patients without ASCVD. Therapies that prevent progression of arterial stiffness and reduce late-systolic pressure overload may help to reduce the prevalence of LV diastolic dysfunction in this population.
Medical treatment for asymptomatic carotid artery stenosis (ACAS) has advanced recently. The outcomes of medical treatment and surgical treatment were evaluated to clarify the optimal treatment for ACAS. Patients with ACAS of ≥ 50% luminal narrowing underwent serial follow-up carotid artery ultrasonography for one year or more at the Center for Cardiovascular Disease Prevention between November 2006 and October 2013. The incidence of cardiovascular events (stroke, myocardial infarction, cardiovascular death) was examined in 64 patients (medical treatment group), and in 47 patients (surgical group) who underwent surgical treatment (carotid endarterectomy or carotid artery stenting) during this same period at the Department of Neurosurgery. Annual cardiovascular event rate was 0.91% (2/219 person-year) in the group of guideline-oriented medical treatment with an annual check-up for disease management and 5.6% (6/107 person-year) in the surgical group (log-rank P = 0.027; HR in the medical treatment group, 0.19 [medical treatment/surgical]; 95% confidence interval [CI], 0.028 to 0.87). Annual stroke event rate was 0.46% (1/219 person-year) in the medical treatment group and 4.7% (5/107 personyear) in the surgical group (log-rank P = 0.016; HR in the medical treatment group, 0.11 [medical treatment/surgical]; 95% CI, 0.0057 to 0.70). Multivariate logistic analysis showed that the surgical group was an independent variable associated with cardiovascular events (P = 0.049). Annual cardiovascular and stroke event rates were low in patients receiving medical treatment for ACAS and better than surgical treatment. The present study shows that medical treatment is an important option for ACAS.
Endovenous laser ablation (EVLA), which is a relatively new therapeutic option for saphenous varicose veins of the legs, is less invasive than conventional stripping surgery with ligation. In this study, we evaluated the safety and effectiveness of EVLA combined with ligation for severe saphenous varicose veins that were graded as ≥ C4 by the CEAP classification. We treated 119 Japanese patients (141 limbs) between July 2005 and December 2007 utilizing a 1320-nm Nd:YAG laser. The obliteration rate of the treated veins was found to be 100% over the entire follow-up period (2.5 years). Consistent with this finding, all of the patients exhibited improved skin lesions (ie, skin pigmentation and ulceration). No major complications, including deep vein thrombosis (DVT) and nerve injury, were observed. A questionnaire survey with a reasonable response rate (66.4%) demonstrated that subjective symptoms and minor complications that were initially observed after EVLA, such as mild pain, numbness, indurations, and localized hot flashes, were remarkably improved by the end of the follow-up period. Furthermore, high levels of patient satisfaction were noted. Thus, EVLA combined with ligation constituted a safe and effective strategy for treating severe saphenous varicose veins in Japanese patients.
Caglar Ozmen, Ali Deniz, Rabia Eker Akilli, Onur Sinan Deveci, Caglar Emre Cagliyan, Halil Aktas, Aziz İnan Celik, Ayca Acikalin Akpinar, Nezihat Rana Disel, Hüseyin Tugsan Balli, İsmail Hanta, Mesut Demir, Ayhan Usal, Mehmet Kanadasi
Pulmonary embolism (PE) is a potentially life-threatening condition and the fact that 90% of PE originate from lower limb veins highlights the significance of early detection and treatment of deep vein thrombosis.1) Massive/high risk PE involving circulatory collapse or systemic arterial hypotension is associated with an early mortality rate of approximately 50%, in part from right ventricular (RV) failure.2) Intermediate risk/submassive PE, on the other hand, is defined as PE-related RV dysfunction, troponin and/or B-type natriuretic peptide elevation despite normal arterial pressure.3) Without prompt treatment, patients with intermediate risk PE may progress to the massive category with a potentially fatal outcome. In patients with PE and right ventricular dysfunction (RVD), in hospital mortality ranges from 5% to 17%, significantly higher than in patients without RVD.4,5)
Exercise could be a therapeutic approach for cardiovascular dysfunction induced by estrogen deficiency. Our previous study has shown that estrogen maintains cystathionine-γ-lyase (CSE) expression and inhibits oxidative stress in the myocardium of female rats. In the present study, we investigated whether exercise improves CSE expression and oxidative stress status and ameliorates isoproterenol (ISO)-induced cardiac damage in ovariectomized (OVX) rats. The results showed that treadmill training restored the ovariectomy-induced reduction of CSE and estrogen receptor (ER)α and decrease of total antioxidant capacity (T-AOC) and increase of malondialdehyde (MDA). The level of CSE was positively correlated to T-AOC and ERα while inversely correlated to MDA. OVX rats showed increases in the serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) and the percentage of TUNEL staining in myocardium upon ISO insult compared to sham rats. Exercise training significantly reduced the serum levels of LDH and CK and the percentage of TUNEL staining in myocardium upon ISO insult in OVX rats. In cultured cardiomyocytes, ISO treatment decreased cell viability and increased LDH release, while overexpression of CSE increased cell viability and decreased LDH release in the cells upon ISO insult. The results suggest that exercise training improves the oxidative stress status and ameliorates the cardiac damage induced by oxidative stress in OVX rats. The improvement of oxidative stress status by exercise might be at least partially due to upregulation of CSE/H2S signaling.
To identify proteins related to the pathophysiology of aortic valve stenosis (AS), we investigated the protein profiles of AS aortic valves. Specifically, proteins were extracted from a thickened and calcified area (AS-C) and an apparently non-thickened and non-calcified area (AS-N) in an identical aortic valve leaflet in each of 6 AS patients. The proteins were then separated by 2-dimensional gel electrophoresis (2DE). Protein spots detected by 2DE were compared between the AS-C and AS-N samples. Protein spots of interest were subjected to protein identification by mass spectrometry. In total, 670 protein spots were detected by 2DE, 28 of which showed more than 1.5-fold different intensity (P < 0.05) between the AS-C and AS-N samples. Proteins were identified in 17 out of the 28 spots. Fibrinogen and lumican were identified in 9 and 3 spots, respectively. Intensity of these 12 spots was lower in the AS-C samples than in the AS-N samples. In the 1D-Western blot analysis, 4 lumican bands (80 kDa, 75 kDa, 65 kDa, and 53 kDa) were detected, of which 2 bands with 80 kDa and 75 kDa showed lower intensity in the AS-C samples than in the AS-N samples. When de-glycosylated protein samples were used in the 1D-Western blot, only a single lumican band with ~40 kDa was detected, indicating that lumican was variously glycosylated and that highly glycosylated lumican molecules were decreased in AS-C. Collectively, insufficient glycosylation of lumican in the thickened and calcified areas of AS aortic valves may be involved in the pathophysiology of AS.
Duchenne muscular dystrophy (DMD) is caused by mutations in the DMD gene which encodes dystrophin protein. Dystrophin defect affects cardiac muscle as well as skeletal muscle. Cardiac dysfunction is observed in all patients with DMD over 18 years of age, but there is no curative treatment for DMD cardiomyopathy. To establish novel experimental platforms which reproduce the cardiac phenotype of DMD patients, here we established iPS cell lines from T lymphocytes donated from two DMD patients, with a protocol using Sendai virus vectors. We successfully conducted the differentiation of the DMD patient-specific iPS cells into beating cardiomyocytes. DMD patient-specific iPS cells and iPS cell-derived cardiomyocytes would be a useful in vitro experimental system with which to investigate DMD cardiomyopathy.
A 48-year-old woman underwent cardiac resynchronization therapy defibrillator implantation. Coronary sinus (CS) venography showed only one adequate anterior branch for a left ventricular lead. We were able to introduce a quadripolar left ventricular lead (Medtronic 4398-88 cm) to the distal portion of the anterior branch. Although phrenic nerve stimulation (PNS) occurred due to distal bipolar pacing (distal 1–mid 2, with 21-mm distance) and proximal pacing (mid 3–proximal 4, distance 21mm), short-spaced bipolar pacing (mid 2-3, distance 1.3 mm) did not induce PNS until 9V pacing. Shared bipolar pacing from each left ventricular electrode (distal 1 to proximal 4) as cathode and a right ventricular (RV) coil as anode resulted in PNS by 3.0V at 0.4 ms. Although quadripolar pacing could avoid PNS by switching the pacing site (ie, from distal bipolar to proximal bipolar), it might not avoid PNS in cases where the phrenic nerve and CS branch are parallel and in close proximity. We found that even though the phrenic nerve and CS branch were parallel and close, short-spaced bipolar pacing could avoid PNS. In conclusion, short-spaced bipolar pacing selected by quadripolar pacing might be beneficial to avoid PNS when the implantable branch is limited.
Trisomy 13 is associated with a variety of congenital anomalies, some of which are life-threatening and related to poor prognosis. Therefore, cardiac surgery is rarely offered to these patients, especially to those with complex cardiac anomalies. We report the case of a neonate weighing 2324 g who was born with severe congenital heart defects. Transthoracic echocardiography revealed the diagnoses of asplenia, single ventricle, aortic stenosis, coarctation of the aorta, hypoplastic aortic arch, and total anomalous pulmonary venous return. She was hemodynamically unstable. Palliative Norwood procedure with right ventricle–pulmonary artery conduit (RV–PA conduit) was performed at the age of 1 day to save her life. On postoperative day 7, chromosome analysis revealed trisomy 13. Echocardiography revealed good heart function; stable hemodynamic status was achieved with minimal amounts of inotropic agents. However, she developed anuria, which did not improve despite situational possible interventions, including peritoneal dialysis and continuous hemodiafiltration. On postoperative day 37, she succumbed to sudden cardiorespiratory failure. Nevertheless, this case indicates that a neonate with trisomy 13 can have a better chance at survival with cardiac surgery such as the Norwood procedure with an RV–PA conduit.
We present the first case of multiple coronary artery-left ventricular micro fistulae complicated with hepatic arteriovenous fistulae (AVF) in an adult patient. Multiple coronary artery fistulae originated from the left anterior descending coronary artery with aneurysmal change. Multiple coronary artery–left ventricular micro fistulae presented on the left ventricular wall and showed significant localized hypertrophic change. Stress and enhanced cardiac magnetic resonance imaging (CMR) revealed myocardial ischemia that could not be detected by stress Tl-201 cardiac scintigraphy, and late patchy gadolinium enhancement (LGE) in the mid-ventricular wall apex. This LGE pattern did not match the typical pattern observed in patients with apical hypertrophic cardiomyopathy. These observations may help distinguish multiple coronary artery-associated myocardial ischemia and hypertrophy from apical cardiomyopathy.