Different clinical characteristics and outcomes of hypertrophic cardiomyopathy with and without hypertension: seeking the truth.

OBJECTIVE: To determine the different clinical characteristics and outcomes of hypertrophic cardiomyopathy (HCM) patients with and without hypertension (HT). METHODS: A total of 696 HCM patients were included in this study and all HCM diagnoses were confirmed by the genetic test. Patients were analyzed separately in the septal reduction therapy (SRT) cohort and the non-SRT cohort. The primary endpoint was cardiovascular death and the secondary endpoint was all-cause death. Outcome analyses were conducted to evaluate the associations between HT and outcomes in HCM. Medications before enrollment and at discharge were collected in the post-hoc analyses. RESULTS: HCM patients without HT were younger, had a lower body mass index, were more likely to have a family history of HCM, and had a smaller left ventricular (LV) end-diastolic diameter than those with HT in both cohorts. A thicker LV wall, a higher level of N-terminal pro-B-type natriuretic peptide, and a higher extent of LV late gadolinium enhancement were additionally observed in patients without HT in the non-SRT cohort. The presence of HT did not alter the distribution pattern of late gadolinium enhancement, as well as the constituent ratio of eight disease-causing sarcomeric gene variants in both cohorts. Outcome analyses showed that in the non-SRT cohort, patients without HT had higher risks of cardiovascular death (HR = 2.537, P = 0.032) and all-cause death (HR = 3.309, P = 0.032). While such prognostic divergence was not observed in the SRT cohort. Further post-hoc analyses in the non-SRT cohort found that patients without HT received fewer non-dihydropyridine calcium channel blockers and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers before enrollment and at discharge. CONCLUSIONS: HCM patients without HT had worse clinical conditions and higher mortality than patients with HT overall, which may result from active medical therapy in HT patients. Active SRT may have a substantial de-risking effect on patients meeting the indications.

Abnormalities of myocardial perfusion and glucose metabolism in patients with isolated left ventricular non-compaction.

BACKGROUND: The prevalence of myocardial perfusion and glucose metabolic abnormalities and their significance in patients with isolated left ventricular non-compaction (ILVNC) have not been well investigated. METHODS: Seventeen ILVNC patients who underwent cardiac magnetic resonance (CMR) and (99m)Tc-sestamibi SPECT/fluorine-18 deoxyglucose ((18)F-FDG) PET imaging were included. Left ventricular non-compaction, regional wall motion abnormalities, left ventricular ejection fraction (LVEF), and delayed enhancement (DE) were estimated using CMR. Myocardial perfusion and metabolism were evaluated with SPECT/PET. RESULTS: Ninety-five (32.9%) segments were considered non-compacted. DE was present in 52 (18.0%) segments and 10 (58.8%) patients. The rate of occurrence of DE was significantly higher in compacted segments than in non-compacted segments (22.7% vs 8.4%, P = .003). Myocardial perfusion abnormalities were present in 92 (31.8%) segments, of which 66 were perfusion/metabolism match and 26 were perfusion/metabolism mismatch. The rate of occurrence of perfusion abnormality was similar between compacted and non-compacted segments (32.0% vs 31.6%, P = .948), but it was significantly higher in segments with DE than in those without DE (51.9% vs 27.4%, P = .001). None of the imaging features alone (non-compaction, DE, perfusion abnormalities, match or mismatch) showed significant correlations with LVEF (all P > .05). CONCLUSION: In the current study, myocardial perfusion/metabolism mismatch and match were observed in both non-compacted and compacted myocardium in ILVNC patients. Further research is warranted to determine their pathologic and clinical significance.

Clinical analysis and risk stratification of ventricular septal rupture following acute myocardial infarction.

BACKGROUND: Ventricular septal rupture (VSR) remains an infrequent but devastating complication of acute myocardial infarction (AMI). The best time to undergo surgical repair is controversial and there is currently no risk stratification for patients with VSR to guide treatment. The purpose of this study was to review the clinical outcomes of 70 patients with VSR, to analyze the short-term prognosis factors of VSR following AMI, and to make a risk stratification for patients with VSR. METHODS: A total of 70 consecutive VSR patients following AMI treated in our hospital from January 2002 to October 2010 were enrolled in this study retrospectively. The difference of clinical characteristics were observed between patients with VSR who survived ≤30 days and survived >30 days. We analyzed the short-term prognosis factors of VSR and established the short-term prognosis index of VSR (SPIV) based on the Logistic regression analysis to stratify patients with VSR. RESULTS: Among 12 354 patients with acute ST-segment elevation myocardial infarction, 70 (0.57%) patients (33 males and 37 females) were found to have VSR. The average age was (68.1±8.5) years. Fifty-four (77.1%) patients were diagnosed with an acute anterior infarction. Patients with VSR selected for surgical repair had better outcomes than patients treated conservatively; 1-year mortality 9.5% versus 87.8%, P < 0.005. Logistic regression analysis revealed that female (P = 0.013), anterior AMI (P = 0.023), non-ventricular aneurysm (P = 0.023), non-diabetes (P = 0.009), Killip class 3 or 4 (P = 0.022) and time from AMI to VSR less than 4 days (P = 0.027) were independent risk determinants for shortterm mortality. SPIV ≥9 indicates a high risk as the 30-day mortality is 77.4%; SPIV <8 indicates a low risk as the 30-day mortality is 28.6%; SPIV between 8 and 9 indicates a moderate risk. CONCLUSIONS: VSR remains a rare but devastating complication of AMI. The independent risk determinants for short-term mortality of VSR were female gender, anterior AMI, non-ventricular aneurysm, non-diabetes, Killip class 3 or 4, and the time from AMI to VSR less than 4 days. It is reasonable to take more active treatments for the patients at high risk to save more lives.

[Short-term prognosis and risk factors of ventricular septal rupture following acute myocardial infarction].

OBJECTIVE: To analyze the short-term prognosis and risk factors of ventricular septal rupture (VSR) following acute myocardial infarction (AMI). METHODS: A total of 70 consecutive VSR patients following AMI hospitalized in our hospital from January 2002 to October 2010 were enrolled in this study. We compared the clinical characteristics of patients with VSR who survived ≤ 30 days (n = 39) and survived > 30 days (n = 31) post AMI. A short-term prognosis index of VSR (SPIV) was established based on the logistic regression analysis. RESULTS: The single factor analysis showed that the risk factors of death within 30 days of VSR patients were female, anterior AMI, Killip class 3 or 4, apical VSR and non-aneurysm (all P < 0.05). Logistic regression analysis revealed that female (P = 0.013), anterior AMI (P = 0.023), non-aneurysm (P = 0.023), non-diabetes (P = 0.009), Killip class 3 or 4 (P = 0.022) and time from AMI to VSR less than 4 days (P = 0.027) were independent risk determinants for death within 30 days post VSR. Patients with SPIV ≥ 9 were associated with high risk [77.4% (24/31)] of dying within 30 days post AMI. SPIV ≤ 8 were associated with low risk as the 30 days mortality is 28.6% (8/28). CONCLUSION: Female gender, anterior AMI, non-aneurysm, non-diabetes, Killip class 3 or 4 and time from AMI to VSR less than 4 days are independent risk factors of short-term mortality of VSR.

[Incidence of coronary artery disease and outcome of patients with left ventricular noncompaction].

OBJECTIVE: To analyze the incidence of coronary artery disease (CAD) and outcome of patients with left ventricular noncompaction (LVNC). METHODS: Fifty-one patients with LVNC evaluated by echocardiography and/or cardiac magnetic resonance (CMR) from January 2006 to August 2010 were retrospectively reviewed. Coronary angiography or MDCT was performed for detecting coronary artery disease. Predictors of the cardiac events were analyzed by Cox regression analysis. RESULTS: There were 31 LVNC patients without CAD and 20 LVNC patients with CAD including single vessel coronary disease in 9 cases, double vessel coronary disease in 3 cases, three vessel coronary disease in 5 cases and left main coronary disease in 3 cases. Coronary artery bypass graft and percutaneous coronary intervention (PCI) were performed in 4 patients. Compared to LVNC patients without CAD, mean age (P = 0.008), incidence of hypertension (65.0% vs. 19.4%, P = 0.001), diabetes mellitus (40.0% vs. 12.9%, P = 0.026) and hyperlipidemia (55.0% vs. 25.8%, P = 0.035) were significantly higher while NT-proBNP level was significantly lower (P = 0.049) in LVNC patients with CAD. Incidence of major cardiac events was similar in LVNC patients with or without CAD. LogNT-proBNP is the independent prognostic factor for adverse cardiac events in patients with LVNC (HR 3.993, 95%CI 1.140 - 13.988, P = 0.030). CONCLUSIONS: Coronary artery disease is common in patients with LVNC and associated with traditional risk factors for CAD. Poor prognosis is associated with increased NT-proBNP but not with CAD in this patient cohort.

Mid-ventricular obstructive hypertrophic cardiomyopathy with apical aneurysm and sustained ventricular tachycardia: a case report and literature review.

The case is a 54-year-old man with hypertrophic cardiomyopathy, mid-ventricular obstruction, apical aneurysm, and recurrence sustained monomorphic ventricular tachycardia (VT). A coronary angiogram revealed myocardial bridging located in the middle of the left anterior descending coronary artery (LAD), and the left ventriculogram showed an hour-glass appearance of the left ventricular cavity. There was a significant pressure gradient of 60 mmHg across the mid-ventricular obliteration at rest. A successful myectomy of the inappropriate hypertrophy myocardium and excision of the apical aneurysm were performed. Pathologic analysis demonstrated fibrosis in the apical aneurysm and thickened and narrowed vessels in the adjacent area. During the follow-up of eighteen months, the patient remained clinically stable and free from arrhythmic recurrence.

[The association study of serum total bilirubin, plasma N-terminal proBNP and invasive hemodynamic parameters in patients with heart failure].

OBJECTIVE: To explore the correlation among serum total bilirubin (TBil), invasive hemodynamic parameters, plasma N-terminal proBNP (NT-proBNP) and C reactive protein (CRP) in patients with heart failure. METHODS: Invasive hemodynamic parameters derived from Swan-Ganz catheter, TBil, plasma NT-proBNP and CRP within 12 hours after hospital admission were analyzed in 130 patients with chronic heart failure [New York Heart Association (NYHA) class II-IV]. RESULTS: Compared with those in non-hyperbilirubinemia group, pulmonary capillary wedge pressure (PCWP), NT-proBNP and left ventriculus ejection fraction were different significantly in total hyperbilirubinemia group [(26.09 vs 16.00) mm Hg (1 mm Hg = 0.133 kPa), (3.36 vs 2.91) pmol/L, (34.12 vs 28.92)%, P < 0.05]. The serum TBil increased significantly in higher PCWP, right atrial pressure and NT-proBNP groups than those in lower level groups [(32.22 vs 24.17), (37.52 vs 24.19), (32.14 vs 16.74) pmol/L, P < 0.05]. Partial correlation analysis showed serum TBil was associated with PCWP, right atrial pressure, pulmonary vascular resistance index and NT-proBNP respectively (r = 0.21, P = 0.02; r = 0.33, P < 0.01; r = 0.20, P = 0.04; r = 0.37, P < 0.01, respectively). Multiple linear regression analysis showed both right atrial pressure and NT-proBNP correlated independently with serum TBil (beta = 0.39, P < 0.01; beta = 0.29, P = 0.01, respectively). CONCLUSION: For patients with heart failure, serum TBil correlated well with right atrial pressure, PCWP and NT-proBNP; it is a reliable indicator for exact clinical evaluation of heart failure.

[Value of admission NT-proBNP in predicting in-hospital mortality in decompensated systolic heart failure].

OBJECTIVE: To evaluate the value of NT-proBNP in predicting in-hospital mortality in patients with decompensated systolic heart failure. METHODS: Plasma NT-proBNP levels within 24 hours of admission were obtained in 366 patients with decompensated systolic heart failure. The levels were compared between dying patients in hospital and survival patients at discharge. ROC analyses were performed to evaluate if NT-proBNP was a predictor for in-hospital mortality and identify the optimal NT-proBNP cut-off point for predicting in-hospital mortality. A binary logistic regression analysis was used to evaluate if NT-proBNP was an independent predictor for in-hospital mortality. RESULTS: 19 cases of the 366 patients died in hospital. NT-proBNP levels of the dying cases were much higher than those of the survivals 3970 (3452, 6934) pmol/L vs 2340 (1132, 4002) pmol/L respectively, P < 0.01). ROC analysis of NT-proBNP to predict in-hospital mortality had an area under the curve (AUC) of 0.762 (95% CI: 0.657-0.857, P < 0.01), the optimal NT-proBNP cut-off point for predicting in-hospital mortality was 3500 pmol/L with a sensitivity of 73.7%, a specificity of 66.9%, an accuracy of 67.6% and a negative predictive value of 97.9%. Patients whose NT-proBNP levels were equal or more than 3500 pmol/L had an in-hospital mortality of 10.9%, compare with 2.1% in those NT-proBNP levels less than 3500 pmol/L (P < 0.01). Binary logistic regression analysis demonstrated that NT-proBNP was an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure (P < 0.01). CONCLUSION: Admission plasma NT-proBNP level is an independent predictor for in-hospital mortality in patients with decompensated systolic heart failure. The optimal NT-proBNP cut-off point for predicting in-hospital mortality is 3500 pmol/L.

[Predictive value of admission amino-terminal pro-B-type natriuretic peptide on in-hospital mortality in patients with decompensated heart failure].

OBJECTIVE: To evaluate the predictive value of admission plasma amino-terminal pro-B-type natriuretic peptide (NT-proBNP) on in-hospital mortality in patients with decompensated heart failure. METHODS: Plasma NT-proBNP levels were measured in patients with decompensated heart failure within 24 hours after admission with ELISA method. The NT-proBNP levels were compared between survivals and dying patients in hospital. ROC analyses were performed to evaluate the predictive value of admission plasma NT-proBNP on in-hospital mortality and to identify the optimal NT-proBNP cut-point for predicting in-hospital mortality. A binary logistic regress analyses was used to evaluate if NT-proBNP was an independent predictor for in-hospital mortality. RESULTS: A total of 804 patients with decompensated heart failure were enrolled in his study (293 valvular heart diseases, 219 ischemic cardiomyopathy, 141 dilated cardiomyopathy, 14 hypertrophic cardiomyopathy, 21 restrictive cardiomyopathy, 39 hypertensive heart disease, 41 chronic pulmonary heart disease and 36 adult congenital heart disease) and 96 patients were in class II, 450 in class III and 258 in cases IV according to NYHA Classification. During hospitalization, 64 deaths were recorded and the on admission plasma NT-proBNP levels of patients died during hospitalization were significantly higher than those of survivals [4321.1 (3063.8, 6606.5) pmol/L vs. 1921.6 (873.9, 3739.2) pmol/L, P<0.01]. Area under receiver operating characteristic curve (AUC) of NT-proBNP to predict in-hospital death was 0.772 (95% CI: 0.718 - 0.825, P<0.01), the optimal plasma NT-proBNP cut-point for predicting in-hospital mortality was 3500 pmol/L, with a sensitivity of 70.3%, a specificity of 72.0%, an accuracy of 71.9%, a positive predictive value of 17. 8% and a negative predictive value of 96.6%. Patients whose NT-proBNP levels were equal or more than 3500 pmol/L had a much higher in-hospital mortality (17.8%) compared with those with NT-proBNP levels of less than 3500 pmol/L (3.4%), P<0.01. Binary logistic regress analyses demonstrated that admission plasma NT-proBNP, pneumonia, heart rate and NYHA class were independent predictors for in-hospital mortality in patients with decompensated heart failure (P<0.05 or 0.01) and admission plasma NT-proBNP was the strongest predictor for in-hospital mortality. CONCLUSIONS: Admission plasma NT-proBNP level was an independent predictor for in-hospital mortality in patients with decompensated heart failure. The optimal NT-proBNP cut-point for predicting in-hospital mortality was 3500 pmol/L in this patient cohort.

[Association of plasma amino-terminal pro-A-, B- and C-type natriuretic peptide levels with NYHA grade and echocardiographic derived parameters of cardiac function in heart failure patients].

OBJECTIVE: To observe the correlation of plasma amino-terminal pro-A-, B- and C-type natriuretic peptide (NT-proANP, NT-proBNP and NT-proCNP) levels with New York Heart Association (NYHA) functional class and echocardiographic derived parameters of cardiac function in heart failure patients. METHODS: Data of NYHA grade, echocardiographic derived parameters of cardiac function, plasma levels of NT-proANP, NT-proBNP and NT-proCNP (measured by enzyme immunoassay method) were obtained in 112 heart failure patients and 44 normal control subjects. The correlation analysis was made between NT-proANP, NT-proBNP, NT-proCNP and NYHA functional class, left atrium diameter (LAD), left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF), respectively. RESULTS: The plasma concentrations of NT-proANP, NT-proBNP and NT-proCNP in heart failure patients were significantly higher than in control group (all P<0.05). Correlation analysis revealed a strong correlation between NT-proANP and NT-proBNP (r = 0.790, P = 0.000) and a weak correlation between NT-proCNP and NT-proBNP (r = 0.278, P = 0.003) as well as between NT-proCNP and NT-proANP (r = 0.236, P = 0.012) in heart failure patients. Univariant analysis showed that NT-proANP and NT-proBNP were positively correlated to LAD, LVEDD and negatively correlated to LVEF (all P<0.05) while there was no significant correlation between NT-proCNP and echocardiographic derived parameters of cardiac function in heart failure patients. Multivariate stepwise regression analysis including age, gender, NYHA classification, LAD, LVEDD and LVEF revealed that NYHA classification, LVEF, LAD and age were independent predictors of NT-proANP; while NYHA classification, LVEF and age were independent predictors of NT-proBNP while there was no association among these factors and NT-proCNP. CONCLUSION: In heart failure patients, the plasma concentration of NT-proANP, NT-proBNP and NT-proCNP were significantly increased and NT-proANP, NT-proBNP but not NT-proCNP were significantly correlated to NYHA classification and echocardiographic derived parameters of cardiac function.

[Association of serum uric acid, plasma NT-proBNP, Hs-C reactive protein and invasive hemodynamic parameters in patients with heart failure].

OBJECTIVE: To explore the correlation of serum uric acid, invasive hemodynamic parameters, plasma N-terminal proBNP (NT-proBNP) and Hs-C reactive protein (Hs-CRP) in patients with heart failure. METHOD: Invasive hemodynamic parameters derived from Swan-Ganz catheter, serum uric acid, plasma NT-proBNP and Hs-CRP within 12 hours after hospital admission were analyzed in 141 patients with chronic heart failure [New York Heart Association (NYHA) class II-IV]. RESULTS: Incidence of hyperuricemia was 55.30% in this patient cohort. Pulmonary capillary wedge pressure (PCWP) and plasma NT-proBNP in hyperuricemia patients were significantly higher than those in non-hyperuricemia patients (P < 0.01). The percentages of high plasma NT-proBNP (> 600 pmol/L) and hyperuricemia were significantly higher in patients with PCWP > or = 18 and < 28 mm Hg (1 mm Hg = 0.133 kPa) and patients with PCWP > or = 28 mm Hg compared those in patients with PCWP < 18 mm Hg, (P = 0.01, P = 0.02; P < 0.01, P < 0.01, respectively). Partial correlation analysis showed that serum uric acid correlated with right atrial pressure, right ventricular pressure, pulmonary arterial pressure and PCWP (r = 0.19, P = 0.03; r = 0.45, P < 0.01; r = 0.23, P = 0.01; r = 0.24, P = 0.01, respectively). Multiple linear regression analysis showed both serum uric acid and plasma NT-proBNP correlated independently with PCWP (beta = 0.24, P = 0.01; beta = 0.47, P < 0.01, respectively) while plasma Hs-CRP and left ventricular ejection fraction were not correlated with serum uric acid and PCWP (P > 0.05). CONCLUSION: Serum uric acid independently correlated with PCWP in patients with heart failure and the combined measurements of serum uric acid and plasma NT-proBNP are helpful in evaluating the prognosis of patients with heart failure.

Nicorandil reduces myocardial no-reflow by protection of endothelial function via the activation of KATP channel.

INTRODUCTION: It has been found that nicorandil can attenuate myocardial no-reflow. However, the exact cause of this beneficial effect has remained unclear. We investigated whether the beneficial effect of nicorandil on myocardial no-reflow could be partly due to its protection against endothelial dysfunction. METHODS: Ligation area and area of no-reflow were determined echocardiographically and pathologically in sixty-two animals randomized into 7 study groups: 9 controls, 9 nicorandil-treated, 8 glibenclamide (K(ATP) channel blocker)-treated, 10 N(G)-monomethyl-L-arginine (L-NMMA, nonselective nitric oxide synthase antagonist)-treated, 10 nicorandil and glibenclamide-treated, 8 nicorandil and L-NMMA-treated and 8 sham-operated. The acute myocardial infarction and reperfusion model was created with one 3-h occlusion of the left anterior descending coronary artery followed by 2 h of reperfusion. Constitutive nitric oxide synthase (cNOS) activity and inducible nitric oxide synthase (iNOS) activity were also quantified. RESULTS: Compared with the control group, nicorandil significantly improved ventricular function, increased coronary blood flow volume (P<0.01), decreased area of no-reflow and reduced necrosis area. Nicorandil also increased the cNOS activity and decreased iNOS activity (P<0.05). L-NMMA and glibenclamide abrogated the effects of nicorandil on ventricular function, coronary blood flow volume, area of no-reflow, necrosis area and cNOS activity, but not iNOS activity. CONCLUSIONS: The beneficial effect of nicorandil on myocardial no-reflow could be due to its protection of endothelial function via the activation of K(ATP) channel.