螺内酯抑制急性前壁心肌梗死患者的左室重构

目的探讨急性前壁心肌梗死患者口服螺内酯对于左室重构的影响。方法将急性前壁心肌梗死患者随机分为两组。对照组30例,接受血管紧张素转换酶抑制剂、β-受体阻滞剂、抗血小板、调脂药物等常规处理。螺内酯组30例,在常规治疗基础上加用螺内酯（40mg,每日1次）。随访1年,并检测脑钠尿肽（BNP）及超声心动图以评价左室功能和左室容积。结果6和12月时螺内酯组血清BNP水平明显低于对照组[（355±74）ng/Lvs（418±77）ng/L,P<0.05和（316±72）ng/Lvs（389±67）ng/L,P<0.05],且12月时螺内酯组较对照组左室舒张末期内径（LVEDD）、左室收缩末期内径（LVESD）明显缩小[LVEDD:（49±6）mmvs（53±5）mm,P<0.05;LVESD:（37±5）mmvs（40±4）mm,P<0.05]。结论螺内酯可抑制急性前壁心肌梗死患者左室重构。     

小剂量螺内酯抑制急性前壁心肌梗死患者的左室重构

目的 探讨小剂量螺内酯对急性前壁心肌梗死患者血清脑利钠肽（BNP）水平和左室重构的影响.方法 选择急性前壁心肌梗死患者90例,在常规治疗基础上,随机分为3组：常规治疗组30例,接受转换酶抑制剂、β受体阻滞剂、抗血小板、调脂药物等常规处理;小剂量螺内酯组30例,在上述治疗基础上每日给予螺内酯20 mg;中剂量螺内酯组30例,在上述治疗基础上每日给予螺内酯40 mg.结果 6个月时小剂量螺内酯组、中剂量螺内酯组和常规治疗组左室射血分数显著升高（P＜0.05）.治疗后常规治疗组BNP水平显著下降（P＜0.05）,小剂量螺内酯组和中剂量螺内酯组BNP水平下降更显著（P＜0.01）;小剂量螺内酯组与中剂量螺内酯组比较差异无统计学意义.结论 小剂量螺内酯抑制急性前壁心肌梗死患者的左室重构,血清BNP水平下降.     

螺内酯对急性心肌梗死患者血浆Ⅲ型前胶原氨基末端肽含量的影响

目的 :探讨螺内酯对急性心肌梗死 (AMI)后血浆Ⅲ型前胶原氨基末端肽 (PⅢNP)的影响。方法 :将6 0例前壁AMI患者随机分为两组 ,对照组采用常规治疗 ,治疗组在常规治疗基础上口服螺内酯 2 5mg ,bid。两组均在入院后第 1、7、2 8、6 0天采血检测PⅢNP含量。结果 :AMI后血清PⅢNP增加 ,与正常人PⅢNP水平相比差异有统计学意义 [(3.2 4± 2 .13)∶(2 .12± 1.78) μg/L ,P <0 .0 5 ]。治疗第 2 8天后 ,治疗组PⅢNP水平明显低于对照组 [(4 .78± 2 .0 1)∶(5 .98± 2 .6 5 ) μg/L ,P <0 .0 5 ]。结论 :在AMI后早期使用螺内酯治疗可以降低PⅢNP含量 ,减少Ⅲ型胶原的产生。     

急性心肌梗死患者血浆Ⅲ型前胶原氨基末端肽与左室重构的关系

目的 :观察急性心肌梗死 (AMI)患者胶原代谢与早期左室重构的相互关系。方法 :AMI患者 32例 ,分为重构组 (18例 )与非重构组 (14例 )。应用放射免疫法测定血浆Ⅲ型前胶原氨基末端肽 (PⅢNP)含量 ,用超声心动图测量左室结构及舒缩功能参数 ,做相关分析 ,并与正常对照组 (30例 )比较。结果 :AMI患者第 4周、第 12周血浆PⅢNP含量分别为 (9.2 3± 3.13) μg/L、(6 .33± 2 .4 1) μg/L ,与第 2天 [(5 .2 2± 1.19) μg/L]及正常对照者[(5 .2 1± 1.18) μg/L]比较明显升高 (均 P <0 .0 1)。重构组第 4周、第 12周血浆PⅢNP含量均明显高于同时间点非重构组含量 (均P <0 .0 1)。第 4周、第 12周血浆PⅢNP含量与左室收缩末期容积呈正相关 (r =0 .4 0 5 ,r=0 .5 13,均P <0 .0 1) ,与二尖瓣血流舒张早期流速 /心房收缩期流速 (r =- 0 .386 ;r =- 0 .35 7,均P <0 .0 1)、左室射血分数 (r =- 0 .4 2 6 ;r =- 0 .346 ,均P <0 .0 1)均呈负相关。结论 :AMI后早期左室重构过程与心肌胶原代谢增强有关 ,血浆PⅢNP含量可作为反映重构过程的有效指标     

螺内酯对急性心肌梗死患者胶原代谢标志物和左室重构的影响

目的:观察螺内酯对急性心肌梗死(AMI)患者胶原代谢标志物及左室重构的影响。方法:将60例AMI患者分为常规治疗组与螺内酯治疗组,应用放射免疫法测定血浆Ⅲ型前胶原氨基末端肽(PⅢNP)、血清透明质酸(HA)含量,用超声心动图测量左室结构及舒缩功能参数。结果:常规治疗组与螺内酯治疗组AMI后第2天血浆PⅢNP分别为(5.24±1.09)、(5.14±1.21)μg/L与正常组[(5.01±1.18)μg/L]相比差异无统计学意义(均P>0.01)。螺内酯治疗组第4周、第12周血浆PⅢNP含量分别为(7.25±1.97)、(6.82±1.98)μg/L较常规治疗组同时间点含量[(10.23±2.25)、(8.36±2.11)μg/L]均显著下降(均P<0.01)。第4周、第12周螺内酯治疗组血清HA含量[(136.4±28.7)、(109.2±30.5)ng/L]与常规治疗组[(167.5±31.5)、(134.5±36.1)ng/L]比较均显著下降(P<0.01)。螺内酯治疗组第12周左室舒张期末容积指数[(57.2±5.8)ml/m2]和收缩期末容积指数[(29.2±5.3)ml/m2]与常规治疗组[(65.9±6.3),(35.7±6.8)]相比均显著降低(P<0.01);二尖瓣血流舒张早期流速(VE)与心房收缩期流速(VA)比值(VE/VA)与常规治疗组相比均显著增加(P<0.01),射血分数虽有增加,但无明显变化(P>0.05)。结论:螺内酯可降低AMI患者血浆PⅢNP、HA含量,阻抑左室重构,改善左室功能。     

溶栓治疗对老年急性心肌梗死患者血清Ⅲ型前胶原末端肽 …

目的　观察溶栓与非溶栓治疗对老年急性心肌梗死 (AMI)患者血清Ⅲ型前胶原水平及左心功能的影响。　方法　将 38例AMI患者分为静脉溶栓组 (2 1例 )和非溶栓组 (17例 ) ,应用放射免疫法测定血清Ⅲ型前胶原末端肽 (PⅢP)含量 ,采用彩色Doppler超声心动图仪测量左室结构及舒缩功能参数。　结果　溶栓组患者在溶栓开始后 1、2、4、6周血清PⅢP含量分别为 (94 35± 11 32 )、(92 2 6± 10 18)、(89 2 4± 8 92 )和 (86 44± 7 98) μg/L ,较同期非溶栓组患者PⅢP(12 4 30± 9 77)、(12 7 6 0± 11 87)、(10 9 80± 10 96 )和 (96 2 0± 9 17) μg/L明显降低 (P <0 0 5或P <0 0 1) ;溶栓未再通组血清PⅢP含量显著高于再通组 (P <0 0 5或P <0 0 1)。血清PⅢP含量与左室重塑 (LVRM)程度有良好的相关性 (r=0 375 1,P <0 0 5 ) ,与左室舒缩功能呈负相关 (r =- 0 485 7,P <0 0 5 ;r =- 0 45 6 8,P <0 0 5 )。　结论　早期实施静脉溶栓治疗能降低血清PⅢP水平 ,减少LVRM发生 ,改善左心功能。     

扩张型心肌病恶性心律失常临床观察

目的探讨扩张型心肌病患者恶性心律失常与左室舒张末期内径(LVDLA)、左室射血分数(LVEF)及血浆心房脑钠肽(BNP)的相关性。方法通过回顾性分析,观察2006年10月到2008年6月72例扩张性心肌病患者,根据动态心电图结果,将其分为恶性心律失常组,非恶性心律失常组及无心律失常组,分别测定各组病人的LVDLA、LVEF、血浆BNP水平。结果恶性心律失常组LVDIA74.52±6.38mm,LVEF27.6±4.7%,BNP1236±103ng/L;非恶性心律失常组LVDIA60.23±4.56mm,LVEF38.6±6.5%,BNP645±76ng/L;无心律失常组LVDIA51.45±6.12mm,LVEF46.2±5.8%,BNP245±81ng/L,各组相比有统计学差异。结论扩张性心肌病恶性心律失常与左室舒张末期内径、左室射血分数直接相关,早期监测血浆BNP水平能预测恶性心律失常的发生。     

急性前壁心肌梗死后梗死相关血管延迟开通对晚期左室重构的影响

目的　探讨急性前壁心肌梗死(AMI)后延迟经皮冠状动脉介入治疗(PCI)使梗死相关动脉(IRA)开通对AMI晚期左室重构的影响。方法　选择64例急性前壁、前间壁及广泛前壁Q波性AMI后病情稳定,发病2~14天,平均(9 .1±2 .3)天冠状动脉造影证实左前降支完全闭塞者,依据是否成功行PCI,分为成功PCI组和对照组,分别于急性期、术后2个月和6个月应用超声心动图随访左室大小、左室功能和室壁活动异常情况,并观察6个月期间心力衰竭事件的发生情况。结果　AMI后2个月两组左室射血分数、左室收缩末期容积指数、左室舒张末期容积指数和室壁活动异常积分与急性期相比差异无统计学意义,急性期和2个月时两组上述各指标之间差异也无统计学意义。6个月时两组左室射血分数和室壁活动异常积分与急性期和2个月相比差异无统计学意义,但对照组左室舒张末期容积指数和左室收缩末期容积指数较急性期明显增大(P<0 .01, P<0. 05 ),且与成功PCI组相比差异有统计学意义(P<0 .01, P<0 .05)。6个月随访期间心力衰竭事件发生率对照组为19%,成功PCI组为2%,但差异无统计学意义。结论　急性前壁AMI后IRA延迟开通能明显减少AMI后晚期的左室重构,而对AMI后早期左室重构的影响不大。延迟PCI可能有利于减少AMI后远期心力衰竭事件的发生。     

螺内酯联合美托洛尔对急性心肌梗死急诊介入治疗后晚期左心室重构的影响

目的探讨急性心肌梗死（AMI）患者直接急诊介入治疗（PCI）后应用螺内酯联合美托洛尔与单用美托洛尔对晚期左心室重构的影响。方法102例AMI患者直接急诊PCI血管再通后,用随机、对照的方法,随机分成治疗组（螺内酯联合美托洛尔）51例和对照组（美托洛尔）51例,在早期（〈24h）,3、6个月末3个时点分别检测两组血清Ⅲ型前胶原氨基末肽（PⅢNP）、脑纳肽（BNP）和醛固酮（ALD）水平,并采用彩色多普勒心动超声仪连续随访并测量、计算左心室形态、构型等多项指标。结果治疗组与对照组比较,3、6个月末血清PⅢNP和BNP显著降低[PⅢNP（ng／L）分别为259．1±60．1比289．3±69．4,P〈0．05;195．2±43．1比222．6±47．4,P〈0．01。BNP（ng／L）分别为334．2±82．5比370．8±72．9,P〈0．05;237．6±67．1比278．6±65．4,P〈0．01]。形态学上,两组左心室均逐渐扩大,6个月末最大,两组差异有统计学意义（P〈O．05）。左心室射血分数同组和两组间对应比较均有明显改善（P〈O．05）。结论AMI直接急诊PCI后应用螺内酯联合美托洛尔,对晚期左心室重构的抑制作用优于单用美托洛尔。     

急性前壁心肌梗死时下壁导联ST段压低的临床意义

目的 :探讨急性前壁心肌梗死合并下壁导联 ST段压低的临床意义。方法 :回顾性分析2 2例首发急性前壁心肌梗死患者的心电图、冠状动脉及左室造影资料。结果 :急性前壁心肌梗死时下壁导联 ( 、 、a VF) ST段下移≥ 0 .0 5 m V组与 <0 .0 5 m V组的 、a VL导联 ST80 值有显著性差异 ( P <0 .0 5 ) ;两组的左前降支 6段 ( LAD6 )或 LAD始部病变的发生率也有显著性差异 ( P <0 .0 5 ) ;下壁导联 ST段压低≥ 0 .0 5 m V对 L AD6 或 LAD始部病变预测价值的敏感性及特异性分别是 : 导联 5 9%、5 0 % ; 导联 83%、70 % ;a VF导联 83%、70 %。结论 :急性前壁心肌梗死时下壁导联ST段压低预示 LAD6 或 L AD始部病变是高前侧壁发生透壁性心肌缺血的“镜像”反应 ,表现为 、a VL导联 ST段抬高 ;它与右冠状动脉、左旋支、多支病变以及胸前导联 ST段抬高程度无关     

Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction

AIMS: In the present study we examined plasma and pericardial fluid ANP and BNP concentrations in postinfarction ventricular dysfunction. The association of peptide levels to left ventricular (LV) dysfunction and to the localization of the myocardial infarction (MI) was studied. METHODS AND RESULTS: Plasma and pericardial fluid samples were obtained from 37 patients undergoing coronary bypass surgery. According to the ECG and preceding coronary angiography, the patients were divided into three groups: previous anterior myocardial infarction (MI) (n=12), previous inferior/posterior MI (n=15) and no history of MI (n=10). When compared to the control group with no MI, the patients with anterior MI had elevated plasma ANP and BNP (134+/-13 vs. 81+/-15 pg/ml, P<0.01 and 95+/-10 pg/ml vs. 26+/-8 pg/ml, P<0.01, respectively) and pericardial fluid BNP (473+/-60 pg/ml vs. 57+/-8 pg/ml, P<0.001) levels. The plasma natriuretic peptide concentrations were not increased in the patients with inferior/posterior MI, but the pericardial fluid BNP concentrations were greater than in the patients with no history of MI (129+/-35 pg/ml vs. 57+/-8 pg/ml, P<0.05). Six of the 12 patients with previous anterior MI had LVEF> or =45%. Despite their normal LV systolic function, these patients had increased plasma and pericardial fluid BNP levels when compared to the group with no history of MI (68+/-18 pg/ml vs. 26+/-8 pg/ml, P<0.05 and 534+/-258 pg/ml vs. 57+/-8 pg/ml, P<0.01, respectively). CONCLUSIONS: Previous anterior myocardial infarction was associated with increased cardiac BNP production even if the LV systolic function was normal (LVEF> or =45%). The high pericardial fluid BNP concentrations in postinfarction patients suggest that the BNP synthesis and release are augmented in the ventricular myocardium independent from the LVEF.     

Cardiac angiotensin-converting enzyme activity in myocardial infarction.

The cardiac renin-angiotensin system is regarded as an important modulator in the infarct heart. Little is known about their presence and regulation in human hearts. We measured angiotensin-converting enzyme (ACE) and renin activities at the aortic root and anterior interventricular vein (AIV) in 51 patients with previous myocardial infarction (MI): anterior wall MI in 31 and inferior wall MI in 20 and 33 control subjects. In the anterior wall MI group, the serum ACE activity was increased significantly in the AIV than in the aortic root (16.2 +/- 5.3 vs 15.3 +/- 5.0 nmol/min/ml, p <0.001), whereas the activity was not different between the aortic root and AIV in the control (14.4 +/- 3.7 vs 14.4 +/- 3.7 nmol/min/ ml) and in the inferior wall MI (16.5 +/- 4.8 vs. 17.0 +/-5.2 nmol/min/ml) groups. On the other hand, there was no significant difference in plasma renin activity between the AIV and aortic root in the 3 groups (control group, 1.0 +/- 0.5 vs 1.0 +/- 0.5 pg/ml/hour; anterior wall MI group, 1.3 +/- 0.8 vs 1.3 +/- 0.8 pg/ml/hour; inferior wall MI group, 1.2 +/- 0.7 vs 1.3 +/- 0.8 pg/ml/ hour). The difference in serum ACE activity between the AIV and aortic root had a significant positive linear correlation with pulmonary capillary wedge pressure (r = 0.606, p <0.001), and had a significant negative linear correlation with left ventricular ejection fraction (r = -0.620, p <0.001) in the anterior wall MI group. Serum ACE activity from the infarct region of the left ventricle was augmented in patients with MI, and the activity was increased in proportion to the severity of left ventricular dysfunction.     

长期小剂量螺内酯治疗对收缩功能中间型心力衰竭的临床疗效

目的:研究长期小剂量螺内酯治疗对收缩功能中间型心力衰竭(HFmrEF)的疗效。方法:100例HFmrEF患者被随机均分为常规治疗组(接受慢性心力衰竭标准治疗)和螺内酯组(在常规治疗组基础上加用小剂量螺内酯),两组均治疗随访2年。观察比较两组治疗前后血压、心率(HR)、血脂、空腹血糖(FBG)、血肌酐(SCr)、血钾(K+)、血浆脑钠肽(BNP)、NYHA分级、舒张功能分级和LVEF,治疗1年后的主要不良心血管事件(MACE)和次要终点事件发生率,以及不良反应情况。结果:与治疗前比较,治疗1年后两组SBP、DBP、HR、血浆TC、LDL-C、FBG、BNP水平、NYHA分级和舒张功能分级均显著降低,LVEF和螺内酯组K+水平显著升高,P均<0.01;与常规治疗组比较,治疗1年后螺内酯组HR[(67.6±6.9)次/min比(61.1±5.5)次/min]、血浆LDL-C[(3.5±0.8)mmol/L比(2.8±0.6)mmol/L]、BNP水平[(491.4±295.5)ng/L比(360.5±226.6)ng/L]、NYHA分级[(2.0±0.7)级比(1.4±0.5)级]和舒张功能分级[(2.2±0.7)级比(1.4±0.5)级]降低更显著,K+水平[(4.2±0.7)mmol/L比(4.9±1.4)mmol/L]和LVEF[(46.1±3.8)%比(47.9±4.1)%]升高更显著,P<0.05或<0.01。治疗1年后,螺内酯组MACE发生率(26.0%比86.0%)和心衰住院率(14.0%比66.0%)均显著低于常规治疗组,P均=0.001。结论:在慢性心力衰竭标准治疗基础上施加小剂量螺内酯可显著提高HFmrEF患者的心功能、降低MACE的发生率,从而降低心衰患者后期住院率。     

Intraoperative Computerized Mapping of Ventricular Tachycardia: Differences Between Anterior and Inferior Myocardial Infarctions

INTRODUCTION: Although direct ventricular tachycardia (VT) surgery has been shown to be effective for treatment of inferior myocardial infarction (MI), the differences in the arrhythmia substrates compared to anterior MI have not been systematically delineated. We sought to compare operative procedures and VT substrates between anterior and inferior MI locations. METHODS AND RESULTS: Computerized mapping was performed in 30 patients with a 128-electrode system using epicardial sock and transatrial left ventricular endocardial balloon arrays, followed by combined endocardial resection and cryoablation. At surgery, there were 51 and 34 different VTs in 18 patients with anterior MI and 12 patients with inferior MI, respectively. The proportion of aneurysms was lower in inferior MI (25% vs 78%, P = 0.008). Total activation times accounted for 65% +/- 23% and 50% +/- 22% of the VT cycle length in anterior and inferior infarcts, respectively (P = 0.005). Complete superficial reentry was identified in 12 VTs related to anterior infarcts and in only two VTs associated with inferior infarction (P = 0.038). Involvement of papillary muscles occurred in two patients with inferior MI. Patients with inferior infarcts received more cryolesions and required epicardial cryolesions or mitral valve replacement more frequently, and their operative mortality was greater (2/12 vs 0/18). Noninducibility rate (89.3%) and 2-year survival (76% +/- 8%) did not differ according to infarct location. CONCLUSION: VT associated with inferior MI can be ablated successfully; however, the substrate is more complex, with frequent participation of intramural layers rendering the ablative procedure more difficult.     

Evaluation of cardiac structure by echoreflectivity analysis in acromegaly: effects of treatment

OBJECTIVES: Cardiac echoreflectivity is a noninvasive tool for evaluating cardiac fibrosis. The present paper aimed to study the modifications of cardiac echoreflectivity in a group of acromegalic patients before and after therapy, and to assess possible correlations with serum levels of procollagen III (PIIINP), a peripheral index of collagen synthesis. DESIGN AND METHODS: Cardiac echoreflectivity (as assessed by analyzing 2-D echocardiograms digitized off-line onto a personal computer) and PIIINP levels were evaluated in 16 acromegalic patients of new diagnosis not affected by arterial hypertension (10 males, six females, age+/-s.d.: 38+/-10 years), and in a group of 16 sex- and age-matched healthy subjects. All the patients were re-evaluated after surgical and/or medical therapy for acromegaly. The echo patterns were analyzed by software that supplies the derived collagen volume fraction (dCVF), an index of fibrosis. RESULTS: At baseline, acromegalic patients showed significantly higher dCVF values and PIIINP levels than healthy controls (3.1+/-0.5% vs 1.6+/-0.3%, P<0.01 and 8.7+/-2.2 vs 3.1+/-1.1 ng/ml, P<0.05, respectively, by unpaired Student's t-test). After therapy, dCVF and PIIINP levels normalized in the six controlled patients (that is, GH of <2.5 microg/l and IGF-I within normal range) (dCVF from 2.8+/-0.4% to 1.4+/-0.2%, P<0.001; PIIINP from 8+/-2.7 to 3.3+/-1.9 ng/ml, P<0.05), while no significant changes were found in noncontrolled patients (dCVF from 3.3+/-0.6% to 2.9+/-1.2% and PIIINP from 9.1+/-1.9 to 7.9+/-3.5 ng/ml, P=NS). A positive correlation between dCVF and PIIINP (r=0.75, P<0.001) and between IGF-I and both dCVF and PIIINP (r=0.65 and 0.61 respectively, P<0.05) was found in acromegalic patients. CONCLUSIONS: Cardiac echoreflectivity, which may be a reflection of heart collagen content, is increased in patients with active acromegaly and correlates with PIIINP concentrations. After cure or adequate control of the disease, both parameters revert to normal. Echoreflectivity analysis could be a useful adjuvant parameter in the assessment of the activity of acromegalic disease.     

醛固酮拮抗剂对老年慢性心力衰竭患者的疗效

目的：探讨长期应用醛固酮拮抗剂（螺内酯）的老年慢性心力衰竭（CHF）患者的左室重构、左室功能与脑钠肽（BNP）水平的关系和临床评价治疗效果。方法：在常规治疗心力衰竭药物治疗的基础上,120例CHF患者采用双盲法随机分为：螺内酯组（66例,螺内酯20mg／d）,CHF常规治疗对照组（54例）;检测治疗前、治疗3个月后左室重量指数（LVMI）、左心室射血分数（LVEF）、脑钠肽（BNP）水平的变化并进行比较分析。结果：螺内酯组心功能改善的总有效率80％,明显高于CHF常规治疗对照组的9．25％,P〈0.05;与CHF常规治疗对照组比较,螺内酯组治疗3月后LVMI[（340．7±68．3）g／m2比（179．6±33．3）g／m2]、BNP[（366．15±23．36）pg／ml比（330．38±11．56）pg／ml]水平显著降低,LVEF[（34．11±2．71）％比（46．2±3．9）％]显著升高（P均〈0．05）。结论：醛固酮拮抗剂在常规治疗心力衰竭的药物治疗的基础上,可降低BNP水平,改善心功能,抑制心室重构。     

Evaluation of procollagen III peptide as a marker of tissue hyperthyroidism in long-term treated women with TSH suppressive doses of thyroxine.

Increased serum concentrations of the aminoterminal propeptide of collagen III (PIIINP) are found in overt hyperthyroidism. Thus, measurement of serum PIIINP might be useful as an early marker of tissue hyperthyroidism in patients with TSH suppressive thyroxine treatment. In a prospective study we evaluated female patients followed in the thyroid outpatient clinic. Serum PIIINP concentrations were analysed in three groups: patients with TSH suppressive thyroxine treatment for more than 6 months (n = 33, TSH < 0.1 mU/l), patients with thyroxine substitution for hypothyroidism for more than 6 months (n = 20, TSH 0.2-4.0 mU/l) and spontaneous hyperthyroid patients (n = 8, TSH < 0.03 mU/l, increased freeT4 and/or T3). Beside TSH, thyroid hormones and serum PIIINP we measured serum SHBG and a clinical score. Hyperthyroid patients had clearly elevated serum PIIINP and SHBG values and a higher clinical score when compared with other study groups (p < 0.001). Patients with TSH suppressive thyroxine treatment had higher fT4 and T3 concentrations than the thyroxine substitution group (fT4 22 +/- 4.8 pmol/l vs. 17 +/- 2.6 pmol/l, T3 2.2 +/- 0.4 nmol/l vs. 1.8 +/- 0.3 nmol/l, p < 0.001) and also elevated serum SHBG values (77.6 +/- 27.5 nmol/l vs. 58.4 +/- 18 nmol/l, p < 0.01). However, serum PIIINP concentrations and the clinical score were very similar in both thyroxine treated groups (PIIINP in TSH suppression group 3.0 +/- 0.67 microg/l vs. 2.8 +/- 0.65 microg/l in the substitution group, clinical score 2 +/- 1.8 pts. vs. 1.7 +/- 1.5 pts. p = n.s.). In conclusion, serum PIIINP is not a reliable early marker for detection of tissue hyperthyroidism in long-term thyroxine treated women with suppressed TSH.     

Valsartan decreases type I collagen synthesis in patients with hypertrophic cardiomyopathy.

BACKGROUND: Fibrosis, as well as myocyte hypertrophy, is the major determinant of prognosis in hypertrophic cardiomyopathy (HCM). Valsartan, an angiotensin II type 1 receptor blocker, may improve myocardial fibrosis in patients with HCM. METHODS AND RESULTS: Twenty-three patients with HCM were randomly divided into 2 groups: 11 patients had valsartan added to conventional treatment (V group) and 12 patients received the conventional therapy (C group). Plasma concentrations of brain natriuretic peptide (BNP), troponin T (TnT), aldosterone (ALDO), procollagen type I (PIP) and procollagen type III aminoterminal peptide (PIIINP) were measured before and 12 months after this study. Left ventricular wall thickness (LVWT) and ejection fraction (LVEF) were measured by echocardiography. PIP was decreased in the V group (123.2+/-63.1 ng/ml to 102.8+/-37.6, p<0.05), but unchanged in C group (110+/-40.5 ng/ml to 119.9+/-47.4, p=0.22). ALDO concentration was unchanged in the V group (88.5+/-26.2 pg/ml to 91.2+/-26.8, p=0.27), and increased in C group (92.6+/-36.6 ng/ml to 116.0+/-33.3, p<0.05). BNP, PIIINP, and TnT were unchanged by the treatment. There was no significant difference between the 2 groups in either LVWT or LVEF. CONCLUSION: Valsartan suppresses the synthesis of type I collagen in patients with HCM and this was associated with suppression of the increase in ALDO.     

Effects of aldosterone receptor blockade in patients with mild-moderate heart failure taking a beta-blocker

AIMS: Spironolactone improves prognosis in severe heart failure (HF). We investigated its effects in patients with mild-moderate HF treated with an ACE inhibitor and beta-blocker. METHODS AND RESULTS: Randomised, double-blind, parallel-group, 3-month comparison of placebo and spironolactone (25 mg daily) in 40 patients in New York Heart Association (NYHA) class I (20%), II (70%) or III (10%), with a left ventricular ejection fraction of <40%. The mean (standard error) changes from baseline in the spironolactone and placebo groups were, respectively: i) B-type natriuretic peptide (BNP) -53.4(22.2) pg/mL and +3.3(12.1) pg/mL, P=0.04, ii) pro-collagen type III N-terminal amino peptide (PIIINP) -0.6(0.2) micromol/L and +0.02(0.2) micromol/L, P=0.02 and iii) creatinine +10.7(3.2) micromol/L and -0.3(2.6) micromol/L, P=0.01. Compared with placebo, spironolactone therapy was associated with a reduction in self-reported health-related quality of life: change in visual analog score: -6 (3) vs. +6 (4); P=0.01. No differences were observed on other biochemical, neurohumoral, exercise and autonomic function assessments. CONCLUSION: In patients with mild-moderate HF, spironolactone reduced neurohumoral activation (BNP) and a marker of collagen turnover (PIIINP) but impaired renal function and quality of life. The benefit-risk ratio of aldosterone blockade in mild HF is uncertain and requires clarification in a large randomised trial.