Effects of intensive blood pressure control on left ventricular hypertrophy in aortic valve disease.

BACKGROUND: Hypertension adds to the pressure overload on the left ventricle (LV) in combination with aortic valve (AV) disease, but the optimal blood pressure (BP) targets for patients with AV disease remain unclear. We tried to investigate whether intensive BP control reduces LV hypertrophy in asymptomatic patients with aortic stenosis (AS) or aortic regurgitation (AR). METHODS: A total of 128 hypertensive patients with mild to moderate AS (n = 93) or AR (n = 35) were randomly assigned to intensive therapy, targeting a systolic BP <130 mm Hg, or standard therapy, targeting a systolic BP <140 mm Hg. The primary end point was the change in LV mass from baseline to the 24-month follow-up. Secondary end points included changes in severity of AV disease, LV volumes, ejection fraction and global longitudinal strain (GLS). RESULTS: The treatment groups were generally well balanced regarding the baseline characteristics. The mean (±SD) age of the patients was 68 ± 8 years and 48% were men. The mean BP was 145 ± 12/81 ± 10 mm Hg at baseline. Medication at baseline was similar between the 2 groups. The 2 treatment strategies resulted in a rapid and sustained difference in systolic BP (P < .05). At 24-month, the mean systolic BP was 129 ± 12 mm Hg in the intensive therapy group and 135 ± 14 mm Hg in the standard therapy group. No patient died or underwent AV surgery during follow-up in either of the groups. LV mass was changed from 189.5 ± 41.3 to 185.6 ± 41.5 g in the intensive therapy group (P = .19) and from 183.8 ± 38.3 to 194.0 ± 46.4 g in the standard therapy group (P < .01). The primary end point of change in LV mass was significantly different between the intensive therapy and the standard therapy group (-3.9 ± 20.2 g vs 10.3 ± 20.4 g; P = .0007). The increase in LV mass index was also significantly greater in the standard therapy group (P = .01). No significant differences in secondary end points (changes in severity of AV disease, LV volumes, ejection fraction and GLS) were observed between the treatment groups. CONCLUSIONS: Among hypertensive patients with AV disease, intensive hypertensive therapy resulted in a significant reduction in LV hypertrophy, although progression of AV disease was similar between the treatment groups. CLINICAL TRIAL REGISTRATION: http://ClinicalTrials.gov (Number NCT03666351).

False-positive supraclavicular lymph node detected on chest computed tomography in oncology patients: Clinical implication based on subsequent neck ultrasonography and ultrasonography-guided tissue sampling.

PURPOSE: The purpose of this study was to assess the prevalence and clinical implications of false-positive supraclavicular lymph node (LN) detected on chest computed tomography (CT), using subsequent neck ultrasonography (US) and US-guided tissue sampling. METHODS: Among 172 patients with suspected supraclavicular LNs identified on CT, 87 underwent neck US or US-guided tissue sampling. Receiver operating characteristic curve and logistic regression analyses were performed to determine the diagnostic performance of US and independent predictors of false-positive LNs. RESULTS: Among 87 patients, 49 (56.3%) were pathologically confirmed as metastases, 26 (29.9%) were negative for malignancy, and 12 (13.8%) had pseudolesions or schwannomas. The diagnostic indices were as follows: sensitivity, 91.8%; specificity, 92.3%; PPV, 95.7%; NPV, 85.7%; and accuracy, 92.0% (AUC = 0.921; 95% CI: 0.832-0.970, p < 0.001). The false-positive group had a higher mean age than the true-positive group (mean age, 69.8 ± 9.2 vs. 63.9 ± 9.8, p = 0.003). Logistic regression analyses revealed that age ≥ 65 years was the only independent predictor of false-positive LNs (OR = 4.391; 95% CI: 1.037-18.582; p = 0.044). CONCLUSION: Subsequent US can be helpful for evaluating suspicious supraclavicular LNs detected on CT to establish appropriate management, especially in older patients.

Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction.

Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-ß and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling.

Different Clinical Features between Definite and Possible Takotsubo Syndrome in a Tertiary Referral Hospital.

BACKGROUND: Although imaging examination to exclude coronary artery disease (CAD) is an indispensable step for a definite diagnosis of takotsubo syndrome (TTS), this step may be overlooked in a substantial proportion of patients with secondary TTS admitted to a tertiary hospital. However, the clinical profiles and outcomes of these patients with "possible TTS" have rarely been investigated. METHODS: Among 420 consecutive TTS patients with characteristic transient ventricular ballooning on repeated echocardiography, 244 patients (58.1%) who underwent an imaging study for CAD were diagnosed with "definite TTS," whereas the remaining 176 were designated with "possible TTS." RESULTS: Overall, hypoxia (67.6%) and dyspnea (55.5%) were predominant presentations. The possible group was characterized by higher prevalence of male gender (46.6% vs. 35.2%, p = 0.019), secondary TTS (97.2% vs. 86.5%, p < 0.001), cancer (43.2% vs. 29.1%, p = 0.003), sepsis (46.0% vs. 32.0%, p = 0.003), and nonapical ballooning pattern (30.7% vs. 21.3%, p = 0.001) with less common ST-segment elevation on electrocardiogram (18.8% vs. 34.0%, p = 0.001). The possible group showed higher frequency of mechanical ventilation (56.2% vs. 40.2%, p = 0.001), pulmonary edema (72.2% vs. 61.5%, p = 0.023), and shock management (70.5% vs. 54.1%, p = 0.001) with similar in-hospital mortality (17.2% vs. 17.0%, p = 0.964). CONCLUSIONS: In real-world clinical practice, coronary evaluation for strict diagnosis of TTS is not frequently feasible. Addition of the possible group without coronary evaluation to the clinical spectrum of TTS would be helpful for fair estimation of clinical implication of TTS.

Head-to-head comparison of prognostic accuracy in patients undergoing noncardiac surgery of dobutamine stress echocardiography versus computed tomography coronary angiography (PANDA trial): A prospective observational study.

BACKGROUND: Dobutamine stress echocardiography (DSE) and coronary computed tomography angiography (CTA) can provide perioperative prognostic information in risk stratification of patients undergoing noncardiac surgery. This study directly compared the prognostic value of DSE and CTA in patients undergoing noncardiac surgery. METHODS: Between 2014 and 2016, 215 patients with more than one clinical risk factor for perioperative cardiovascular (CV) events were enrolled prospectively. They received both DSE and CTA before noncardiac surgery. Perioperative clinical risk was classified according to the revised cardiac risk index (RCRI), DSE results were categorized as abnormal (inducible ischemia and/or nonviable infarction) or not. CTA results were assessed using the severity of stenosis, with significant stenosis being ≥50% of the luminal diameter). After the exclusion, a total of 206 patients remained. Perioperative CV events were defined as CV death, non-fatal myocardial infarction (MI), myocardial injury, pulmonary edema, non-fatal stroke, and systemic embolism within 30 days after surgery. RESULTS: Twenty-four patients (12%) had perioperative cardiac events (1 cardiac death, 10 non-fatal MI, 8 myocardial injury, 11 pulmonary edema, 1 non-fatal stroke, and 1 pulmonary embolism). Following adjustment for baseline RCRI score, abnormal result on DSE (OR, 6.08, 95% CI, 2.41 to 15.31, P < 0.001), significant CAD on CTA (OR, 18.79; 95% CI, 5.24 to 67.42, P < 0.001), and high CACS (OR, 4.19; 95% CI, 1.39 to 12.60, P = 0.011) remained significant predictors of perioperative CV events. CONCLUSIONS: DSE and CTA are independent predictive factors of events in patients undergoing noncardiac surgery. Among them, assessment of significant CAD using CTA might show a higher prognostic value compared with DSE before noncardiac surgery. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02250963.

Mid-term Clinical Outcomes in a Cohort of Asymptomatic or Mildly Symptomatic Korean Patients with Bicuspid Aortic Valve in a Tertiary Referral Hospital.

BACKGROUND: Although bicuspid aortic valve (BAV) is one of the most common congenital heart diseases, clinical outcome data regarding BAV are still limited. We evaluated clinical characteristics and mid-term clinical outcomes of asymptomatic Korean patients with bicuspid aortic valve. METHODS: We initiated a prospective registry in 2014 at a tertiary referral hospital. To develop a cohort of asymptomatic patients, we excluded patients who previously underwent open heart surgery (OHS) or who had OHS within 6 months of referral. RESULTS: A total of 170 patients (117 male [69%], age 50 ± 13 years) were enrolled. More than 70% (n = 124, 73%) were incidentally diagnosed with BAV during routine health examinations or preoperative screening for non-cardiac surgery. At the time of enrollment, moderate to severe aortic stenosis (AS) or regurgitation (AR) was present in 77 patients (45%) and 98 (58%) showed aortic dilation: 42 (25%) had non-significant valvular dysfunction without aortic dilation. During a median follow-up of 4 years, AS severity increased significantly (p < 0.001), while there was no significant change in AR severity (p = 0.361). A total of 27 patients (16%) underwent OHS, including isolated aortic valve (AV) surgery (n = 11, 41%), AV with combined aortic surgery (n = 12, 44%), and isolated aortic surgery (n = 4, 15%): no patient developed aortic dissection. Moderate to severe AS (hazard ratio [HR] 4.61; 95% confidence interval [CI] 1.83-11.62; p = 0.001), NYHA class ≥ 2 (HR 2.53; 95% CI 1.01-6.35; p = 0.048) and aortic dilation (HR 2.13; 95% CI 0.87-5.21; p = 0.099) were associated with surgical events. CONCLUSIONS: Progression patterns of valvular dysfunction and impacts of BAV phenotype on OHS should be explored in future studies with longer follow-up durations.

Impact of Significant Mitral Regurgitation on Assessing the Severity of Aortic Stenosis.

BACKGROUND: Significant mitral regurgitation (MR) may reduce a pressure gradient of aortic stenosis (AS) by decreasing forward stroke volume. The study objective was to evaluate whether significant MR can cause inconsistency when assessing the severity of AS. METHODS: Among 5,355 patients diagnosed with AS from 2000 to 2015, 68 were retrospectively found to have concomitant significant (moderate or greater) MR and normal left ventricular ejection fractions in normal sinus rhythm (AS with MR). As a control group, 136 patients with trivial or no MR were selected who were matched by age, gender, and left ventricular end-systolic volume (AS without MR). Nonlinear regression was performed for data pairs (aortic valve area [AVA] vs mean pressure gradient [MPG]) using the formula AVA = a + b/√MPG. Composite clinical events were defined as aortic valve surgery warranted by the development of symptoms or left ventricular dysfunction, admission because of heart failure, and death. RESULTS: The forward stroke volume index was significantly lower in the AS with MR group than in the AS without MR group (43.8 ±â€¯8.3 vs 49.2 ±â€¯10.2 mL/m2, P < .004). A significant group difference was found with respect to the relationship between (indexed) AVA and MPG (AVA, 0.02 + 4.43/√MPG vs -0.06 + 5.60/√MPG [P for interaction = .04]; indexed AVA, 0.03 + 2.66/√MPG vs -0.03 + 3.47/√MPG [P for interaction = .01]). An AVA of 1.0 cm2 corresponded to MPGs of 20.3 and 28.2 mm Hg for the groups with and without MR, respectively. Conversely, an MPG of 40 mm Hg corresponded to AVAs of 0.72 and 0.83 cm2 for the groups with and without MR, respectively. Among patients with MPGs < 40 mm Hg, clinical event rates were significantly higher in those with MR compared with those without MR (P = .009). CONCLUSIONS: This quantitative analysis demonstrated that AS severity assessed by MPG measurement may be underestimated, and thus AVA measurement is essential in patients with combined significant MR.

Performance of a Simplified Dichotomous Phenotypic Classification of Bicuspid Aortic Valve to Predict Type of Valvulopathy and Combined Aortopathy.

BACKGROUND: A simplified classification of bicuspid aortic valve (BAV) morphology using only the orientation of fused cusps was recently proposed. The aim of this study was to test whether it is useful for showing an association with the type of valvulopathy or aortopathy. METHODS: BAV phenotype was retrospectively classified in 681 patients (mean age, 59 ± 12 years; 424 men) who underwent aortic valve surgery. Each BAV was classified using both dichotomous (right and left coronary cusp fusion [CCF] vs mixed cusp fusion [MCF]) and conventional methods, and its association with the dominant valvulopathy (aortic stenosis [AS] vs regurgitation) and concomitant aortic surgery was analyzed. Four cardiologists individually reviewed transthoracic echocardiographic images of 100 randomly selected patients to compare the feasibility and accuracy of the two classification methods. RESULTS: The frequencies of BAV CCF and MCF were 53% (n = 361) and 47% (n = 320), respectively. AS was the predominant cause of surgery (n = 546 [80%]), and concomitant aortic surgery was done in 31% (n = 214). Patients with BAV MCF showed a higher frequency of AS (89% vs 73%, P < .001) and aortic surgery (38% vs 26%, P < .001) than those with BAV CCF. There were independent associations between BAV MCF and AS (odds ratio, 3.32; 95% CI, 1.99-5.54; P < .001) as well as aortic surgery (odds ratio, 1.76; 95% CI, 1.26-2.45; P = .001). The feasibility of the classification methods did not differ, but dichotomous classification revealed higher accuracy than conventional (87% [95% CI, 84.1%-90.7%] vs 70% [95% CI, 65.0%-74.3%]) for all four examiners, with higher κ coefficients representing interrater agreement (κ = 0.73 ± 0.06 to 0.83 ± 0.06 [dichotomous method] vs 0.51 ± 0.06 to 0.73 ± 0.06 [conventional method]). CONCLUSIONS: The dichotomous classification method is useful for showing the association with the type of valvulopathy or aortopathy, with better diagnostic performance than the conventional method.

Antiplatelet Therapy Combinations and Thrombogenicity in Patients with Non-Valvular Atrial Fibrillation.

BACKGROUND AND OBJECTIVES: Combination antiplatelet therapy reduces the risk of ischemic stroke compared with aspirin monotherapy in non-valvular atrial fibrillation (NVAF) patients. The underlying mechanism, however, remains unclear. In addition, the association between platelet inhibition and thrombogenicity in NVAF has not been evaluated. SUBJECTS AND METHODS: We randomized 60 patients with NVAF that were taking 100 mg of aspirin daily (>1 month) to adding 75 mg of clopidogrel daily (CLPD group), 100 mg of cilostazol twice daily (CILO group), or 1000 mg of omega-3 polyunsaturated fatty acid twice daily (PUFA group). Biomarkers (von Willebrand factor antigen [vWF:Ag], fibrinogen, D-dimer, and high-sensitivity C-reactive protein [hs-CRP]) and platelet reactivity (PR), which were the levels stimulated by adenosine diphosphate (ADP), thrombin-receptor agonist peptide, collagen, and arachidonic acid, were measured at baseline and 30-day follow-up. RESULTS: Combination antiplatelet therapy significantly reduced vWF:Ag and fibrinogen levels (7.7 IU/dL, p=0.015 and 15.7 mg/dL, p=0.005, respectively), but no changes were found in D-dimer and hs-CRP levels. The CLPD and CILO groups showed fibrinogen and vWF:Ag level reductions (24.9 mg/dL, p=0.015 and 9.3 IU/dL, p=0.044, respectively), whereas the PUFA group did not show any differences in biomarkers. Irrespective of regimen, the changes in fibrinogen and vWF:Ag levels were mainly associated with the change in ADP-mediated PR (r=0.339, p=0.008 and r=0.322, p=0.012, respectively). CONCLUSION: In patients with NVAF, combination antiplatelet therapy showed reductions for vWF:Ag and fibrinogen levels, which may be associated with the inhibitory levels of ADP-mediated PR. The clinical implications of these findings need to be evaluated in future trials.

Novel role of platelet reactivity in adverse left ventricular remodelling after ST-segment elevation myocardial infarction: The REMODELING Trial.

The role of platelet-leukocyte interaction in the infarct myocardium still remains unveiled. We aimed to determine the linkage of platelet activation to post-infarct left ventricular remodelling (LVR) process. REMODELING was a prospective, observational, cohort trial including patients (n = 150) with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. Patients were given aspirin plus clopidogrel therapy (600 mg loading and 75 mg daily). Platelet reactivity (PRU: P2Y12 Reaction Units) was assessed with VerifyNow P2Y12 assay on admission. Transthoracic echocardiography was performed on admission and at one-month follow-up. The primary endpoint was the incidence of LVR according to PRU-based quartile distribution. LVR was defined as a relative ≥ 20 % increase in LV end-diastolic volume (LVEDV) between measurements. Adverse LVR was observed in 36 patients (24.0 %). According to PRU quartile, LVR rate was 10.8 % in the first, 23.1 % in the second, 27.0 % in the third, and 35.1 % in the fourth (p = 0.015): the optimal cut-off of PRU was ≥ 248 (area under curve: 0.643; 95 % confidence interval: 0.543 to 0.744; p = 0.010). LVR rate also increased proportionally according to the level of high sensitivity-C reactive protein (hs-CRP) (p = 0.012). In multivariate analysis, the combination of PRU (≥ 248) and hs-CRP (≥ 1.4 mg/l) significantly increased the predictive value for LVR occurrence by about 21-fold. In conclusion, enhanced levels of platelet activation and inflammation determined the incidence of adverse LVR after STEMI. Combining the measurements of these risk factors increased risk discrimination of LVR. The role of intensified antiplatelet or anti-inflammatory therapy in post-infarct LVR process deserves further study.

Comparison of Results of Tricuspid Valve Repair Versus Replacement for Severe Functional Tricuspid Regurgitation.

The optimal decision regarding whether to repair or replace the tricuspid valve (TV) remains controversial in patients with very severe functional tricuspid regurgitation (TR). We sought to compare clinical outcomes of TV repair versus replacement for very severe TR associated with severe TV tethering. We included 96 consecutive patients (20 men, 58 ± 11 years of age) who had both severe tethering of TV and very severe functional TR and consequently underwent TV surgery during left-sided valve surgery. TV repair was performed on 79 patients (repair group), whereas 17 patients underwent TV replacement (replacement group). The primary end point of the study was defined as the composite of operative mortality, cardiac death, repeat TV surgery, and hospitalization due to congestive heart failure during follow-up. The 2 groups had similar baseline clinical, echocardiographic, and operative characteristics, but operative mortality was significantly higher in the replacement group than in the repair group (p = 0.008). During a median follow-up of 87 months, 19 patients (24%) in the repair group and 8 (47%) in the replacement group attained the composite end point, and TV replacement was independently associated with end points in the Cox proportional hazards analysis after adjustment with propensity score (hazard ratio 4.033, 95% CI 1.470 to 11.071; p = 0.007). In conclusion, compared with TV repair, replacement was associated with higher operative mortality and worse long-term clinical outcomes in patients with very severe functional TR. Repair should be the preferred surgical option even for severe TR associated with more advanced tethering and right ventricular dilatation.

Dipeptidyl Peptidase-4 Induces Aortic Valve Calcification by Inhibiting Insulin-Like Growth Factor-1 Signaling in Valvular Interstitial Cells.

BACKGROUND: Calcification of the aortic valve leads to increased leaflet stiffness and consequently to the development of calcific aortic valve disease. However, the underlying molecular and cellular mechanisms of calcification remain unclear. Here, we identified that dipeptidyl peptidase-4 (DPP-4, also known as CD26) increases valvular calcification and promotes calcific aortic valve disease progression. METHODS: We obtained the aortic valve tissues from humans and murine models (wild-type and endothelial nitric oxide synthase-deficient-mice) and cultured the valvular interstitial cells (VICs) and valvular endothelial cells from the cusps. We induced osteogenic differentiation in the primary cultured VICs and examined the effects of the DPP-4 inhibitor on the osteogenic changes in vitro and aortic valve calcification in endothelial nitric oxide synthase-deficient-mice. We also induced calcific aortic stenosis in male New Zealand rabbits (weight, 2.5-3.0 kg) by a cholesterol-enriched diet+vitamin D2 (25 000 IU, daily). Echocardiography was performed to assess the aortic valve area and the maximal and mean transaortic pressure gradients at baseline and 3-week intervals thereafter. After 12 weeks, we harvested the heart and evaluated the aortic valve tissue using immunohistochemistry. RESULTS: We found that nitric oxide depletion in human valvular endothelial cells activates NF-κB in human VICs. Consequently, the NF-κB promotes DPP-4 expression, which then induces the osteogenic differentiation of VICs by limiting autocrine insulin-like growth factor-1 signaling. The inhibition of DPP-4 enzymatic activity blocked the osteogenic changes in VICs in vitro and reduced the aortic valve calcification in vivo in a mouse model. Sitagliptin administration in a rabbit calcific aortic valve disease model led to significant improvements in the rate of change in aortic valve area, transaortic peak velocity, and maximal and mean pressure gradients over 12 weeks. Immunohistochemistry staining confirmed the therapeutic effect of Sitagliptin in terms of reducing the calcium deposits in the rabbit aortic valve cusps. In rabbits receiving Sitagliptin, the plasma insulin-like growth factor-1 levels were significantly increased, in line with DPP-4 inhibition. CONCLUSIONS: DPP-4-dependent insulin-like growth factor-1 inhibition in VICs contributes to aortic valve calcification, suggesting that DPP-4 could serve as a potential therapeutic target to inhibit calcific aortic valve disease progression.

Fabry Disease Presenting with Hypertrophic Cardiomyopathy and Tricuspid Regurgitation.

A 71-year-old female who was diagnosed with nonobstructive hypertrophic cardiomyopathy since 1999 presented with dyspnea and severe edema on both legs. For the management of her symptom, cardiac surgery including tricuspid annuloplasty, Maze operation and right atrial reduction plasty was performed. During follow-up after cardiac surgery, a plasma α-galactosidase activity was checked for the screening of Fabry disease and the result was around lower normal limit. DNA analysis was implemented for confirmation and it revealed a heterozygote α-galactosidase mutation at exon 6 [c.901C>T (p.Arg301Ter)]. This case suggests that Fabry disease might be easily undetected, and clinical suspicion is critical.

Effect of rosuvastatin on coronary flow reserve in patients with systemic hypertension.

Although statins reduce cardiac events in hypertensive patients with cardiovascular risk factors, the effect of statins on coronary flow reserve (CFR) has not been examined. We tried to examine the effect of rosuvastatin on CFR in hypertensive patients at cardiovascular risk. CFR was studied in 56 hypertensive patients (40 men, 61 ± 9 years) with cardiovascular risk factors and without coronary artery disease in a prospective clinical trial. Using Doppler echocardiography, coronary flow velocity in the distal left anterior descending artery was recorded at baseline and during intravenous adenosine infusion, and CFR was defined as the ratio of hyperemic to basal average peak diastolic flow velocity. The primary efficacy measure was defined as the change in CFR after rosuvastatin therapy for 12 months. CFR was measured successfully in 55 of 56 enrolled patients (98%). CFR was 3.16 ± 0.44 at baseline and negatively correlated with age (R = -0.30, p = 0.025). All patients continued rosuvastatin 10 mg/day without any serious adverse events. After rosuvastatin therapy, serum total cholesterol, low-density lipoprotein cholesterol, and high-sensitivity C-reactive protein significantly decreased from 222 ± 18 to 142 ± 20 mg/dl, 148 ± 21 to 85 ± 18 mg/dl, and 1.7 ± 2.9 to 1.2 ± 3.1 mg/L, respectively (all p <0.01). CFR significantly increased from 3.16 ± 0.44 to 3.31 ± 0.42 (p <0.001). The change in CFR correlated with the change in low-density lipoprotein cholesterol (R = -0.28, p = 0.040) but not with the change in high-sensitivity C-reactive protein. In conclusion, CFR was significantly improved after 12 months of rosuvastatin therapy in hypertensive patients at cardiovascular risk and average levels of serum cholesterol.

Prognostic implications of initial echocardiographic findings in adolescents and adults with supracristal ventricular septal defects.

BACKGROUND: Although surgery is recommended for pediatric patients with supracristal ventricular septal defects (sVSDs) to prevent progression of aortic regurgitation (AR), outcomes in adolescents and adults with sVSDs are not known. METHODS: In this retrospective observational study, clinical data without surgery were obtained in 60 patients with sVSDs (group 1; mean age, 36 ± 13 years), 120 age- and defect size-matched patients with perimembranous ventricular septal defects (group 2), and 52 patients with sVSDs who underwent surgery (group 3; mean age, 32 ± 11 years). RESULTS: Aortic sinus wall prolapse (38% vs 3%, P < .0001) and moderate to severe AR (7% vs 0%, P = .012) were more frequently observed in group 1 than in group 2. Five, three, and two patients in group 1 had surgery during follow-up because of rupture of the aneurysm of the sinus of Valsalva, endocarditis, and heart failure, respectively. Group 1 had a lower 12-year clinical event-free (surgery and endocarditis) rate (76 ± 9% vs 94 ± 4%, P = .031) but an equivalent overall survival rate (100% vs 94 ± 3%, P = .143) compared with group 2. Patients with maximal prolapsing aortic sinus wall length > 7 mm showed a higher frequency of aneurysm of the sinus of Valsalva rupture than those with no prolapse or maximal prolapsing length ≤ 7 mm (80% [four of five] vs 2% [one of 55], P < .001). The event-free and overall survival rates were comparable between groups 1 and 3, with equivalent 10-year AR progression-free survival rates (94 ± 5% vs 91 ± 5%, P = .301). CONCLUSIONS: Aneurysm of the sinus of Valsalva rupture, rather than AR progression, was the main clinical event. Watchful monitoring of patients with high-risk echocardiographic features may be a rational option.