Clinical Outcomes of Myocardial Bridging versus No Myocardial Bridging in Patients with Apical Hypertrophic Cardiomyopathy.

OBJECTIVE: To determine the prevalence and clinical effects of myocardial bridging (MB) in patients with apical hypertrophic cardiomyopathy (AHCM). METHODS: Angiograms from 212 AHCM patients were reviewed to identify MB. The patients were classified into 2 groups: AHCM with and AHCM without MB. We reviewed patient records on cardiovascular (CV) risk factors, symptoms, CV events, and CV mortality. RESULTS: In all, 60 patients with MB and 100 without MB were included. Rates of angina (61.7 vs. 40%; p = 0.008), mimicking non-ST-segment elevation myocardial infarction (15 vs. 3%, p = 0.013), and Canadian Cardiovascular Society class III/IV angina (18.3 vs. 4%; p = 0.003) were higher in patients with MB than in those without. Mean follow-up periods (65.5 ± 50.5 vs. 64.4 ± 43.6 months, p = 0.378) and CV mortality (3.3 vs. 1%; p = 0.652) were similar in the 2 groups. Kaplan-Meier estimates demonstrated that CV event-free survival rates were lower in patients with MB than in those without (71.7 vs. 88%; p = 0.022). MB, late gadolinium enhancement, and female sex were independent risk factors for CV events in a multivariate Cox regression analysis adjusted for other risk factors. CONCLUSION: More serious symptoms and a higher risk of CV events were observed in AHCM patients with MB than in those without MB. CV mortality was similar in these 2 groups.

Effectiveness of Alcohol Septal Ablation Versus Transaortic Extended Myectomy in Hypertrophic Cardiomyopathy with Midventricular Obstruction.

OBJECTIVES: Investigate the effectiveness of alcohol septal ablation (ASA) and transaortic extended myectomy (TEM) in hypertrophic cardiomyopathy (HCM) with midventricular obstruction (MVO). BACKGROUND: MVO is less common than subaortic obstruction. Data on the effectiveness of ASA and TEM in MVO are lacking. METHODS: The clinical profiles of 22 patients undergoing ASA and 37 patients undergoing TEM were compared. No patient had apical aneurysm, abnormal chordae, mitral valve replacement or repair. RESULTS: Baseline midventricular pressure gradient and symptoms were comparable between the ASA and TEM groups. During follow-up, both groups demonstrated substantial reduction in pressure gradient (the ASA group: 79.7 ± 21.2 mm Hg to 43.7 ± 28.9 mm Hg, P < 0.001; the TEM group: 69.0 ± 23.9 mm Hg to 15.0 ± 16.9 mm Hg, P < 0.001). The reduction in pressure gradient was greater (78.9 ± 18.6% vs. 46.4 ± 33.4%, P < 0.001) and the residual pressure gradient was lower after TEM versus ASA (P < 0.001). Patients with New York Heart Association class III/IV dyspnea decreased from 59.1 to 18.2% (P = 0.022) in the ASA group and from 56.8 to 5.6% (P < 0.001) in the TEM group. Patients with Canadian Cardiovascular Society class III/IV angina decreased from 40.9 to 9.1% (P = 0.016) in the ASA group and from 32.4 to 0% (P < 0.001) in the TEM group. CONCLUSIONS: While ASA and TEM both improve gradients and symptoms, TEM may provide a more reliable reduction in gradients compared to ASA.

Efficacy and safety of cryobiopsy versus forceps biopsy for interstitial lung diseases and lung tumours: A systematic review and meta-analysis.

Forceps biopsy (FB) is the most commonly used diagnostic tool for lung pathologies. FB is associated with a high diagnostic failure rate. Cryobiopsy (CB) is a novel technique providing a larger specimen size, few artefacts, more alveolar parts and superior diagnostic yield. CB, however, has drawbacks such as higher bleeding and pneumothorax rate. We conducted a meta-analysis to investigate the specimen area, diagnostic rate and bleeding severity in CB versus FB in interstitial lung diseases (ILDs) and lung tumours. A systematic literature search of PUBMED, BIOSIS PREVIEW and OVID databases was conducted using specific search terms. Eligible studies including RCTs and non-RCTs comparing cryobiopsy/cryotransbronchial biopsy (CB/CTBB) and forceps biopsy/forceps transbronchial biopsy (FB/FTBB) for specimen area, diagnostic rate and bleeding rate in ILDs and lung tumours were analysed. Two reviewers independently extracted data and evaluated the quality of the studies. Eight studies involving 916 patients were analysed. Specimen area (mm(2) ) was significantly larger in CB/CTBB than FB/FTBB (standard mean difference = 1.21, 95% confidence interval (0.94, 1.48), P < 0.00001). The diagnostic rate was significantly higher in CB/CTBB than FB/FTBB (Risk ratio 1.36, 95% confidence interval (1.16, 1.59), P = 0.0002). Three studies compared the bleeding severity with only one showing significantly more bleeding in CB. Cryobiopsy/cryotransbronchial shows superiority to FB/FTBB for specimen area and diagnostic rate. CB/CTBB has better efficacy over FB/FTBB.

Incidence of ischemic stroke and systemic embolism in patients with hypertrophic cardiomyopathy, nonvalvular atrial fibrillation, CHA2DS2-VASc score of ≤1 and without anticoagulant therapy.

Data on the risk of ischemic stroke and systemic embolism (iSSE) events in patients with nonvalvular atrial fibrillation (NVAF), a CHA2DS2-VASc score of ≤1, hypertrophic cardiomyopathy (HCM), and without anticoagulant therapy are still lacking. The aim of this study was to investigate the incidence of iSSE events in these patients. We consecutively screened medical records of patients with HCM and NVAF referred to Fuwai Hospital between January 1994 and March 2014. The primary end point was iSSE events, defined as a composite of ischemic stroke and systemic embolism. Follow-up was carried out to ascertain end point status. Medical records of 522 patients with NVAF and HCM were screened. A total of 108 patients (20.7 %) with a CHA2DS2-VASc score of ≤1 and without anticoagulant therapy were enrolled and constituted our study population. After a median follow-up of 2.4 years (range 0.6-14.1 years; 376.2 patient-years), ischemic stroke occurred in 2 patients, resulting in death of 1 patient in the first year and paralysis of the other patient in the fourth year. No other iSSE events occurred. The incidence of iSSE was 0.9 % [95 % confidence interval (CI) 0.0-5.0 %] in the first year, and 0.5 % per 100 patient-years (95 % CI 0.1-1.9 %). The risk of iSSE events seems low in patients with NVAF, a CHA2DS2-VASc score of ≤1, HCM, and without anticoagulant therapy. Multicenter studies with sizeable study populations are needed to validate the risk of iSSE events in these patients.

CT Characteristics and Clinical Findings of Bronchopneumonia Caused by Pepper Aspiration.

Purpose: To explore the computed tomography (CT) features of bronchopneumonia caused by pepper aspiration to improve the diagnosis. Materials and Methods: 28 adult patients diagnosed with obstructive pneumonia caused by pepper aspiration from January 2016 to September 2022 were enrolled. The CT characteristics of bronchial changes and pulmonary lesions caused by pepper were analyzed and summarized. Results: Among 28 patients, the most common symptom was cough (26, 92.9%), followed by expectoration (23, 82.1%). Bronchoscopy revealed that peppers were mainly found in the bronchus of the right lower lobe (n = 18, 64.3%), followed by the bronchus of the left lower lobe (n = 5, 17.9%). In combination with bronchoscopy results, the pepper in the bronchus manifested as circular or V/U-shaped high-density, localized soft tissue, and flocculent opacification in 8 (28.6%), 16 (57.1%), and 3 (10.7%) cases on CT images, respectively. The bronchial wall around the pepper was thickened with localized occlusion (n = 19, 67.9%) and stenosis (n = 9, 32.1%). Regarding adjacent bronchi without peppers, extensive wall thickening with stenosis and/or occlusion was found in 23 (82.1%) cases. Distal pulmonary lesions frequently involved two or three segments (21, 75.0%) and mainly presented as patchy consolidation or atelectasis (24, 85.7%). Conclusion: In combination to a history of eating peppers and clinical symptoms, bronchopneumonia caused by pepper should be highly suspected if U/V-shaped and annular high-density or localized soft tissue density is detected in the bronchi of the lower lobes, accompanied by extensive bronchial wall thickening, stenosis, or occlusion, and consolidation or atelectasis in multiple distal lung segments.

[Theory and application of pulse diagnosis at Renying and Cunkou regions].

Renying and Cunkou pulse diagnostic method is one of the important parts of the pulse diagnosis in Huangdi Neijing (Inner Canon of Yellow Emperor) and has been controversial since its proposal. This article takes WANG Shu-he's diagnostic operation as the evidence, and is in reference of the statement, "Cun region (the region ahead of Guan region of Cunkou) determines the human life, that on the left hand refers to Renying, while on the right hand is Qikou". The pulse conditions on the left and right hands represent yin and yang. If Renying pulse on the left is greater, the diseases are in yang meridians, while if Cunkou pulse on the right is bustling, the diseases are in yin meridians. By comparing the pulse condition and strength, as well as the pulse beating (rapid and urgent) between Guan region and region ahead of Guan on the same side, the conditions of three yang and three yin meridians are detected. In treatment, based on the records of Renying and Cunkou pulse diagnosis in Huangdi Neijing, the principles are proposed for reinforcing and reducing methods on hand and foot meridians of yin and yang. Five-shu points and yuan-source points are taken as the main acupoints in acupuncture treatment. During treatment, the changes in pulse conditions should be emphasized specifically and those at Renying and Cunkou regions are the criteria for judging qi arrival and qi regulation.

IL-11 drives the phenotypic transformation of tracheal epithelial cells and fibroblasts to enhance abnormal repair after tracheal injury.

Tracheal stenosis (TS) is a multifactorial and heterogeneous disease that can easily lead to respiratory failure and even death. Interleukin-11 (IL-11) has recently received increased attention as a fibrogenic factor, but its function in TS is uncertain. This study aimed to investigate the role of IL-11 in TS regulation based on clinical samples from patients with TS and a rat model of TS produced by nylon brush scraping. Using lentiviral vectors expressing shRNA (lentivirus-shRNA) targeting the IL-11 receptor (IL-11Rα), we lowered IL-11Rα levels in the rat trachea. Histological and immunostaining methods were used to evaluate the effects of IL-11Rα knockdown on tracheal injury, molecular phenotype, and fibrosis in TS rats. We show that IL-11 was significantly elevated in circulating serum and granulation tissue in patients with TS. In vitro, TGFß1 dose-dependently stimulated IL-11 secretion from human tracheal epithelial cells (Beas-2b) and primary rat tracheal fibroblasts (PRTF). IL-11 transformed the epithelial cell phenotype to the mesenchymal cell phenotype by activating the ß-catenin pathway. Furthermore, IL-11 activated the atypical ERK signaling pathway, stimulated fibroblasts proliferation, and transformed fibroblasts into alpha-smooth muscle actin (α-SMA) positive myofibroblasts. IL-11-neutralizing antibodies (IL-11NAb) or ERK inhibitors (U0126) inhibited IL-11 activity and downregulated fibrotic responses involving TGFß/SMAD signaling. In vivo, IL-11Rα knockdown rats showed unobstructed tracheal lumen, relatively intact epithelial structure, and significantly reduced granulation tissue proliferation and collagen fiber deposition. Our findings confirm that IL-11 may be a target for future drug prevention and treatment of tracheal stenosis.

Efficacy and safety of aranidipine enteric-coated tablets compared with amlodipine in Chinese patients with mild to moderate essential hypertension: a multicenter, randomized, double-blind, parallel-controlled clinical trial.

This is a multicenter, randomized, double-blind, parallel-controlled study, conducted in Chinese patients with mild to moderate essential hypertension. After a 2-week washout period, 236 eligible patients were randomly to receive aranidipine 5-10 mg/d (n = 118) or amlodipine 5-10 mg/d (n = 118) for 10 weeks. The blood pressure and heart rate were evaluated in outpatient clinics, and ambulatory blood pressure monitoring was performed in 24 patients in each group. The blood pressure was significantly decreased in both groups. Compared with amlodipine, the patients who received aranidipine had less response in blood pressure (P < 0.01). The trough/peak ratios of diastolic blood pressure in aranidipine and amlodipine groups were 0.57 ± 0.20 and 0.68 ± 0.19, respectively (P = 0.119). Adverse events occurred at 11.86% and 7.63% in the aranidipine and amlodipine groups, respectively (P = 0.348). Headache was observed at an incidence of >3.0% in both groups, and the serum glucose and lipid profile had no significant change in the amlodipine group. In conclusion, once-daily administration of aranidipine (5-10 mg) effectively controlled blood pressure, and the short-term treatment might result in it being less effective than amlodipine. It had a stable action over 24-hour period, and the mechanism of that is not yet clear. Aranidipine had a good safety similar to that of amlodipine.

[Modeling of systolic blood pressure reaction to antihypertensive agents in people with hypertension].

OBJECTIVE: We used the individual patient data from clinical trials, pooled in the INDANA data set, to explore whether blood pressure reduction was related to the baseline individual characteristics, and quantify the potential associations. METHODS: We used the data from 31 140 patients with essential hypertension recruited in four randomized placebo-controlled clinical trials, MRC35-64, MRC65-74, STEP and SYST-EU. Thiazide diuretics, ß-blocker, and calcium channel blocker, three of six major BP lowering drugs were analyzed. Patients were all with the same first dosage of the drug in each trial. Age, body weight, height, level of total cholesterin (TC), systolic blood pressure (SBP) and diastolic blood pressure (DBP) when initialed and at first visit of follow-up, pharmacological treatment, gender, status of smoking, history of myocardium infarction were factors taken into model. Data were managed by software SAS(®). Statistical analyses were performed with SAS(®) and R. Model was developed to evaluate the relationship between decrease of SBP and characteristics of patients. RESULTS: Initial SBP is the only modifier of treatment effect on SBP response in the 3 BP lowering drug classes (ß = 0.09, 0.37 and 0.18, respectively). Age and initial DBP were factors significantly correlated with SBP fall for diuretic (ß = 0.17 and 0.14), and age was one of factors significantly correlated with SBP fall for ß-blocker (ß = -0.17). Smokers would receive less SBP fall compare to non-smokers in ß-blocker active treated group (ß = -2.07). There is converse effect of age between the diuretic and ß-blocker; older people seem sensitive to diuretic, while young people are sensitive to ß-blocker. As to calcium channel antagonist class, body weight is another modifier (ß = 0.06) (All P value are 0.000 except 0.050 for body weight in calcium channel antagonist class). CONCLUSION: We identified 5 significant modifiers (baseline SBP and DBP, age, smoking status and body weight) for SBP response to treatment effect, while gender, TC and history of myocardial infarction are not modifiers for SBP response to treatment effect.

[Clinical features and prognosis of 188 Chinese patients with apical hypertrophic cardiomyopathy].

OBJECTIVE: To analyze the clinical characteristics and prognosis of Chinese patients with apical hypertrophic cardiomyopathy (AHCM). METHODS: A total of 188 patients with AHCM diagnosed at Fuwai Hospital were included in this retrospective study. Clinical characteristics, mortality and cardiovascular morbidity were analyzed. A multiple logistic regression was performed to adjust for potential confounding factors. RESULTS: Males predominated with a number of 139 (73.9%) in this cohort. Patient's age ranged from 15 to 81 (51.9 ± 12.6) years. There were 120 patients (63.8%) with "pure" type and 68 patients (36.2%) with "mixed" type of AHCM, 171 patients were followed up for (5.0 ± 3.0) years, cardiovascular mortality was 1.2%, 28 patients (16.4%) experienced one or more cardiovascular events. CONCLUSION: The prevalence of AHCM is high in Chinese HCM patients, pure type AHCM is more common, and AHCM patients have a benign clinical course.

[Comparison of benazepril monotherapy to amlodipine plus benazepril in the treatment of patients with mild and moderate hypertension: a multicentre, randomized, double-blind, parallel-controlled study].

OBJECTIVE: To evaluate the efficacy and tolerability of the fixed combination of amlodipine 5 mg/benazepril 10 mg once-daily therapy, compared with benazepril, 10 mg, monotherapy in patients with mild and moderate hypertension, and to evaluate the 24 h antihypertensive efficacy and the duration of action by ambulatory blood pressure monitoring. METHODS: In a multicenter, randomized, double-blind, parallel controlled trial, 356 cases of hypertensive patients after 2 weeks wash-out, and then given 4 weeks of benazepril 10 mg monotherapy, 220 patients with mean seated diastolic blood pressure (SeDBP) remained ≥ 90 mm Hg (1 mm Hg = 0.133 kPa) were randomly divided into benazepril 10 mg/amlodipine 5 mg (BZ10/AML5) fixed-dose combination therapy group (once a day, n = 113), and benazepril monotherapy group (daily 20 mg, n = 107). In the two groups the patients with SeDBP ≥ 90 mm Hg were doubled the dosage of the initial regimen at the end of 4-week treatment for additional 4 weeks, and the patients with SeDBP < 90 mm Hg remained the initial regimen for additional 4 weeks. The primary endpoint was to evaluate the improvement of SeDBP at the end of 8-week treatment. There were 74 patients (the combination therapy group n = 38, monotherapy therapy group n = 36) completed the 24 h ambulatory blood pressure monitoring which was included in the final efficacy analysis. RESULTS: The randomized, double-blind treatment for 8 weeks, the mean value of SeDBP reduction, the reaching target blood pressure rate and total successful response rate to the treatment (a SeDBP < 90 mm Hg or a decrease of 10 mm Hg or more from baseline) were (11.7 ± 6.8) mm Hg, 65.7% and 88.5% in the combination therapy group, respectively, and were (7.7 ± 6.9) mm Hg, 35.5% and 65.5% in the monotherapy group, respectively. There were statistically significant difference between the combination therapy and the monotherapy groups in all the 3 indexs (P < 0.001). The fixed combination significantly reduced systolic blood pressure (SBP) and diastolic blood pressure (DBP) values throughout the 24 h. The trough to peak ratios of DBP/SBP in the fixed compound of benazepril/amlodipine (10 mg/5 mg) and benazepril (20 mg) alone were 83.1%/76.0% and 85.8%/79.5%, respectively. Adverse events rates were 16.8% in the combination therapy group and 35.5% in the monotherapy group (P < 0.001). CONCLUSIONS: The combination therapy with benazepril/amlodipine was superior to benazepril monotherapy and was well tolerated in patients with essential hypertension and allowing a satisfactory BP control for 24 hours.

Successful management of isolated pulmonary Langerhans cell histiocytosis in a 50-year-old man with early diagnosis using transbronchial cryobiopsy: A case report.

RATIONALE: Isolated pulmonary Langerhans cell histiocytosis (PLCH) is rare in adults. The gold standard diagnosis requires surgical lung biopsy. However, few cases have been diagnosed with transbronchial cryobiopsy (TBCB) sampling in the early stages of the disease, particularly in China. PRESENTING CONCERNS: A 50-year-old man was referred for dry cough and exertional dyspnea of more than 1 week. High-resolution computed tomography (HRCT) of the chest revealed symmetric nodules and cyst lesions with upper lobe infiltrate. Further history taking indicated that he had smoked 20 cigarettes per day for more than 30 years. Therefore, PLCH was highly suspected. However, he refused surgical lung biopsy, and TBCB was attempted to complete diagnosis. DIAGNOSIS: Emission computed tomography excluded the possibility of extrapulmonary involvements, and pathological findings supported the diagnosis of isolated PLCH. INTERVENTIONS: Smoking cessation and prednisone treatment were used for patient management. OUTCOMES: The symptoms receded with significant improvement of chest HRCT during 2-months of follow-up. LESSONS: Early diagnosis contributes to the prognosis of isolated PLCH in adults, and TBCB may be an alternative to conventional surgical lung biopsy for pathological diagnosis of PLCH.

Rapid response to lipids profile and leukocyte gene expression after rosuvastatin administration in Chinese healthy volunteers.

BACKGROUND: Statins are potent lipid-lowering agents widely used in medical practice. There has been growing evidence suggesting the pleiotropic effects of statins in addition to the lipid-lowering effect. However, it is still unclear how rapidly the beneficial effects of statins occur. The transcriptome of peripheral blood cells can be used as a sensor to drug therapy. The purpose of the study was to investigate the acute effects of rosuvastatin both on lipids profile and gene expression of peripheral leukocytes following therapy with a single dose of rosuvastatin. METHODS: Thirty healthy Chinese male volunteers were enrolled. The serum lipids, high-sensitivity C-reactive protein, and plasma fibrinogen were determined before and 72 hours after administration of 20 mg of rosuvastatin. The differentially expressed genes of peripheral leukocytes after administration of rosuvastatin were screened using human oligonucleotide microarray gene expression chips. Then four of the differentially expressed genes including ATM, CASP8, IL8RB and S100B were verified by real-time polymerase chain reaction (PCR). RESULTS: Rosuvastatin decreased both serum total cholesterol and low-density lipoprotein cholesterol significantly 72 hours after administration of a single dose of 20 mg rosuvastatin. However, no significant changes occurred in blood high-density lipoprotein cholesterol, triglycerides, C-reactive protein and fibrinogen after the treatment. A total of 24 genes were differentially expressed after the treatment. They were involved in important cell biological processes such as cytokine-cytokine receptor interaction, apoptosis signaling, etc. CONCLUSIONS: Rosuvastatin rapidly modulates the serum lipids and affects the gene expression of peripheral leukocytes in healthy volunteers. This finding provides some new clues for further studies on its potential pleiotropic effects.

Reduction of C-reactive protein by a single 80 mg of simvastatin in patients with unstable angina.

BACKGROUND: Increased concentrations of C-reactive protein (CRP) became widely accepted as a risk factor of the higher incidence of coronary events, and rapid lowering CRP by administration of drugs may produce early benefit to the coronary endothelium in patients with coronary heart disease and reduce angina and coronary events after revascularization. Limited information has been available, however, with respect to evaluating a potential effect of a single high-dose simvastatin on CRP in patients with unstable angina (UA) within 48 h. We investigated whether a rapid CRP reduction can be achieved by a single 80 mg of simvastatin therapy in patients with UA given immediately on admission. METHODS: Forty-two patients with rest chest pain were randomly assigned to a single placebo or 80 mg of simvastatin given at the time of admission plus standard therapy. Blood samples were also drawn at the time of admission, and 48 h later for measuring serum CRP concentrations. RESULTS: We found that 80 mg of simvastatin induced significant reductions in serum median CRP concentrations and in mean CRP concentrations 48 h later following administration of simvastatin (25.4% and 32.7%, p<0.001, respectively). CONCLUSIONS: A single high-dose simvastatin, given in the early time on admission, is an effective therapy for controlling inflammatory response in patients with UA, and the benefit to the vascular endothelium might occur quickly by reduction of CRP concentrations in this high-risk subgroup.

Effect of arotinolol on left ventricular function in patients with idiopathic dilated cardiomyopathy.

OBJECTIVE: To evaluate the efficacy and safety of long-term treatment with arotinolol in patients with idiopathic dilated cardiomyopathy (IDCM). METHODS: Sixty-three patients with IDCM were evaluated at baseline and after 12-month therapy with arotinolol. The conventional therapy for congestive heart failure was continued throughout the study with arotinolol as the only beta-blocker. Left ventricular function was assessed with the New York Heart Association functional class and two-dimensional echocardiography. RESULTS: After 12-month arotinolol treatment, there was a significant improvement in left ventricular systolic function. Left ventricular end-systolic dimension significantly decreased from 59.52 +/- 8.83 mm to 50.89 +/- 8.17 mm (P < 0.001). Left ventricular ejection fraction significantly increased from 27.39% +/- 7.94% to 41.13% +/- 9.45% ( P < 0.001). Left ventricular mass index decreased from 150.47 +/- 42.42 g/m2 to 141.58 +/- 34.36 g/m2 (P < 0.01). No adverse events leading to premature discontinuation of study drug occurred. CONCLUSION: In this preliminary study, 12-month arotinolol treatment has a favorable effect on left ventricular function in patients with IDCM, and it is safe and well tolerated.

[Efficacy of monotherapy with 15 antihypertensive agents in treating essential hypertension assessed by 24-hour ambulatory blood pressure monitoring].

OBJECTIVE: To evaluate the efficacy of the monotherapy of 15 agents in treating essential hypertension. METHODS: After 2-week wash-out, a total of 370 patients with seated diastolic blood pressure 95-114 mmHg and seated systolic blood pressure < 180 mmHg were randomized to different therapeutic groups. 24-hour ambulatory blood pressure monitoring was performed before medication and at the end of 8 weeks. RESULT: All the agents significantly reduced the 24 hour mean blood pressures after treatment except doxazosin, terazosin, and torasemide. CONCLUSION: The result suggested that the angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers and long-acting calcium antagonists were effective in treating essential hypertension, while the low-dose doxazosin, terazosin and torasemide can be used for combination therapy but not for monotherapy.

Long-term survival after acute myocardial infarction in patients with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is associated with poor prognosis. It has been reported that there is no difference in in-hospital mortality after acute myocardial infarction (AMI) between patients with and without HCM. However, whether there is a difference in long-term survival after AMI between patients with and without HCM remains unclear. HYPOTHESIS: Long-term survival after AMI is worse in patients with vs without HCM. METHODS: The clinical profiles of 91 consecutive patients with HCM and AMI (HCM group) and 91 sex- and age-matched patients with AMI without HCM (non-HCM group) were analyzed. The study endpoint was all-cause mortality. RESULTS: During a follow-up period of 4.9 ± 3.6 years, all-cause mortality occurred in 25 patients (27.5%) in the HCM group and 13 patients (14.3%) in the non-HCM group. The survival of the HCM group was inferior to that of the non-HCM group (log-rank P = 0.039). During the first year of follow-up, 3 deaths (3.3%) occurred in the HCM group and 7 deaths (7.7%) occurred in the non-HCM group (log-rank P = 0.177). Among patients who survived beyond the first year of follow-up (172 patients), the annual mortality rates were 6.3% (95% confidence interval: 4.0%-9.3%) in the HCM group and 1.6% (95% confidence interval: 0.6%-3.5%) in the non-HCM group (log-rank P = 0.001). CONCLUSIONS: AMI patients with HCM exhibited worse long-term survival than did AMI patients without HCM.

Changes of plasma inflammatory markers after withdrawal of statin therapy in patients with hyperlipidemia.

BACKGROUND: Atherosclerosis has been considered to be an inflammatory process. In addition to its lipid-lowering properties, statin has been shown to decrease the concentrations of inflammatory markers resulting in reduction of cardiovascular events. Emerging data suggest that withdrawal of statin might be associated with increased cardiac events. The mechanism for this phenomenon, however, is still unclear. We investigated whether acute termination of statin treatment could result in rebound of inflammatory markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6), in patients with hyperlipidemia. METHODS: Seventeen patients (11 men and 6 women, mean age 51+/-7 years) with hyperlipidemia were given 40 mg/day of pravastatin for 6 weeks. The concentrations of plasma CRP and IL-6 were evaluated before receiving the statin therapy, immediately after 6 weeks of pravastatin therapy, and at days 1, 3 and 7 after withdrawal of pravastatin therapy. The lipid profile was also evaluated at baseline, 6 weeks of therapy, and at day 7 after terminating pravastatin. RESULTS: Pravastatin therapy induced significant reductions in total cholesterol (TC, 6.88+/-0.36 vs. 5.27+/-0.23 mmol/l, p<0.01), low-density lipoprotein (LDL) cholesterol (4.28+/-0.25 vs. 3.06+/-0.14 mmol/l, p<0.01), CRP (0.28+/-0.16 vs. 0.20+/-0.08 mg/l, p<0.01), and IL-6 (8.4+/-0.6 vs. 6.7+/-0.4 pg/dl, p<0.01). Although the TC and LDL-cholesterol did not change during the 7-day period after withdrawal of pravastatin therapy, the concentrations of CRP and IL-6 increased at day 3 (CRP: 0.20+/-0.08 vs. 0.27+/-0.12 mg/l, and IL-6: 6.7+/-0.4 vs. 7.7+/-0.6 pg/dl, p<0.05 respectively) and at day 7 (CRP: 0.20+/-0.08 vs. 0.30+/-0.14 mg/l, and IL-6: 6.7+/-0.4 vs. 8.7+/-0.8 pg/dl, p<0.01 respectively) after withdrawal of pravastatin therapy. No correlation between increase of CRP as well as IL-6 and small changes of LDL-cholesterol concentrations was found after withdrawal of pravastatin therapy at day 7 (r=-0.021 and r=-0.044 respectively, p>0.05 respectively). CONCLUSIONS: 6 weeks after pravastatin therapy could significant modify the lipid profile and decrease the inflammatory markers including CRP and IL-6 in patients with hyperlididemia. Moreover, statin therapy discontinuation could induce a rebound phenomenon of inflammatory response representing an increase in some inflammatory markers, which is independent of changes of lipid parameters.

Rebound phenomenon of inflammatory response may be a major mechanism responsible for increased cardiovascular events after abrupt cessation of statin therapy.

Inflammation has been recognized as having an important role in the development and progression of atherosclerosis. Statins reduce cardiovascular events mainly by cholesterol lowering. A large number of investigations have demonstrated that administration of statin could modify inflammatory response with a concurrent fall in cardiovascular events. Despite the known benefit of statin therapy, many cardiac patients abruptly discontinue therapy because of financial constraints, forgetfulness, or side effects. More recently, several studies have shown that abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. However, the mechanisms of the increased incidence of cardiovascular events after abruptly stopping statin therapy are still unknown. A few data suggest that abrupt withdrawal of statin therapy deteriorates endothelial function, result in expression of pro-inflammatory gene involved in the development and progression of atherosclerosis. We hypothesis that rebound phenomenon of inflammatory response may be a major mechanism responsible for increased cardiovascular events after abrupt cessation of statin therapy. Our very recent data showed that abrupt termination of statin therapy resulted in a rapid increased C-reactive protein (CRP) and interleukin-6 (IL-6) levels in patients with hypercholesterolemia. This finding may be of important interest in the connection between inflammatory response and abrupt withdrawal of statin therapy in patients with coronary artery disease.

Inflammation: a possible pathogenic link to cardiac syndrome X.

Cardiac syndrome X is defined as a typical angina pectoris, positive treadmill exercise test, negative intravenous ergonovine test and normal coronary angiography. The pathogenesis of cardiac syndrome X has previously ascribed to myocardial ischemia that may be caused by microvascular dysfunction and increased sensitivity to intracardiac pain. Despite the extensive studies, the pathophysiological mechanisms in cardiac syndrome, however, remain unclear. More recently, the data has been suggested that chronic inflammation has been associated with cardiac syndrome X. The evidence for the hypotheses included that inflammatory marker are increased, and associated with the disease activity in patients with cardiac syndrome X. And also, statin, a lipid-lowering as well as anti-inflammatory drug, has significantly modified the disease process in this special syndrome. Despite the good prognosis of cardiac syndrome X, the chronic, frequent nature of the persistent angina and reduced exercise tolerance can significantly impair quality of life. Thus, lowering inflammatory response by, for example, use of statin and/or aspirin, might improve coronary microvascular dysfunction. Whether this is a valid approach, however, is still unknown and deserves further investigation. Indeed, as mediators of inflammation are multiple, the strategy of identifying triggers and mechanisms of inflammation in each special clinical setting and directing treatment at the special triggers or to rate limiting steps in effector pathways appears more reasonable or a promising strategy.