血浆Hcy与急性心肌梗死预后关系的临床研究

目的探讨血浆高同型半胱氨酸(Hcy)血症与急性心肌梗死(AM I)预后的关系。方法102例AM I患者分为高Hcy血症AM I组及Hcy正常AM I组,比较两组临床事件(泵衰竭、休克、心律失常、死亡)发生情况及梗死面积等。同时选择健康体检者25例为正常对照组,检测Hcy浓度并与AM I患者进行比较。结果AM I患者血浆Hcy浓度〔(28.29±5.14)μmol/L)〕明显高于正常对照组〔(10.66±2.75)μmol/L)〕(P<0.01);高Hcy AM I组梗死面积、病死率、心律失常、休克及泵衰竭发生率均高于Hcy正常AM I组(P<0.05);冠脉造影显示高Hcy血症与病变血管总数成正相关;多元回归分析表明高Hcy血症是强的心血管事件发生的预测因子(P<0.05)。结论高Hcy血症的AM I患者临床事件发生率明显增多,血管病变程度较Hcy正常者严重,高Hcy血症是AM I心血管事件发生的预测因子。     

Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure

Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 +/- 1.0, 2.5 +/- 0.9 and 2.6 +/- 0.8 hours, respectively), volume of distribution (1.9 +/- 0.7, 1.8 +/- 0.4 and 1.8 +/- 0.5 liters/kg, respectively), clearance (11.3 +/- 7.5, 9.3 +/- 3.6 and 9.1 +/- 3.5 ml/min per kg, respectively) and unbound drug fraction (66 +/- 9, 66 +/- 9 and 69 +/- 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 micrograms/ml in patients with acute myocardial infarction and 3.3 micrograms/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.     

Effect of propranolol after acute myocardial infarction in patients with congestive heart failure

The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictors and importance of congestive heart failure in patients with acute inferior myocardial infarction

Inferior myocardial infarction (MI) is considered to have a more favorable prognosis than anterior wall MI but includes high risk groups with increased mortality and morbidity. It is well known that congestive heart failure (CHF) complicating acute MI has poor prognosis. In this study we assessed the clinical and prognostic significance of CHF and the predictive value of the baseline demographic and clinical variables for CHF in patients with acute inferior MI. A total of 350 patients with acute inferior MI were included. In group A there were 26 patients (7.4%) with CHF, and in group B there were 324 patients (92.6%) without this complication. Baseline clinical and demographic characteristics and in-hospital complications of the groups were assessed. In group A patients were older (67.6±9.5 vs 53.7±10.9 years, p<0.0001) and there were more female patients (50% vs 15%, p<0.00001) compared to group B. The prevalence of diabetes mellitus (58% vs 16%) and precordial ST segment depression on admission ECG (81% vs 50%) were significantly higher in group A compared to group B (p<0.00001 and p=0.002 consecutively). In group A there was a higher rate of righ ventricular (25% vs 23%), posterior (26% vs 24%) and posterolateral myocardial infarction (19% vs 14%), but the differences were not statistically different. In group A patients had significantly higher rate of second- or third-degree AV block (46% vs 8%, p<0.00001), cardiogenic shock (35% vs 1%, p<0.00001) and mortality (46% vs 3%, p<0.00001) compared to group B. In a multivariate regression analysis diabetes mellitus (p=0.0003) and precordial ST segment depression on admission ECG (p=0.002) were found as the independent predictors of in-hospital CHF in patients with acute inferior MI. CHF and ST segment depression on admission ECG were found as the independent predictors of in-hospital mortality (p<0.00001, p=0.04 consecutively). Patients with CHF complicating acute inferior MI have more unfavorable demographic and clinical characteristics on admission, higher rate of in-hospital complications and mortality. History of diabetes mellitus and precordial ST segment depression on admission ECG have an independent predictive value for CHF in this particular group of patients.     

Relationship between plasma atrial natriuretic factor and opioid peptide levels in healthy subjects and in patients with acute congestive heart failure

We evaluated plasma atrial natriuretic factor (ANF), ß-endorphin,met-enkephalin, dynorphin and noradrenaline levels in 20 healthysubjects and 20 acute congestive heart failure (CHF) patients.In all acute CHF patients plasma values of these hormones werehigher than in healthy subjects. The hormonal pattern differedin patients with the more severe acute CHF (group 1) from patientswith less severe acute CHF (group 2) (ANF 53.8 ± 1.0vs 34.6 ± 1.5 pg.ml^–1, noradrenaline 563.8 ±13.4 vs 202.4 ± 10.6 pg.ml^–1, met-enkephalin 41.0± 3.2 vs 17.0 ± 1.6 fmol. ml^–1, dynorphin46.8 ± 3.7 vs 25.2 ± 2.0 fmol. ml^–1, P <0.01;ß-endorphin 50.6 ± 5.2 vs 41.8 ± 4.1fmol. ml^–1, ns). Administration of an opioid antagonist(naloxone, 8 mg i.v.) did not modify ANF or noradrenaline concentrationin healthy subjects. in group 1 naloxone administration significantlyraised ANF (68.0 ± 1.4 pg. ml^–1), noradrenaline(776.6 ± 18.7 pg. ml^–1), blood pressure and heartrate, whereas in group 2 it significantly decreased ANF values(21.9 ± 0.5 pg. ml^–1)and did not modify the otherparameters. Our findings suggest that the opioid system affectsANF release in acute CHF. In patients with severe CHF opioidpeptides may attenuate ANF secretion reducing noradrenergicstimulation. On the other hand, when CHF is less severe andthe sympathetic activity is moderate, opioid peptides may directlystimulate ANF secretion.     

慢性心力衰竭患者血清锌水平与患者预后的关系

目的 研究慢性心力衰竭（chronic heart faliure, CHF）患者血清Zn含量与其预后的关系。 方法 收集院内慢性心力衰竭CHF患者337例相关临床资料，并对患者血清Zn含量进行测定，并测定患者心脏功能以及运动负荷；对所有患者进行为期1年的随访，记录患者随访期内死亡情况。 结果 以患者Zn离子水平分为3组:①72 μg/dl（高水平组，n=112）；②60≦Zn≦71 μg/dl（中水平组，n=112）；③ ≦ 60 μg/dl（低水平组，n=113）。3组患者间年龄、慢性肾衰竭及贫血的患病率、患者利尿剂的使用率、血清Ca、Fe、低密度脂蛋白胆固醇（LDL-C）、超敏C反应蛋白（hs-CRP)、脑钠尿肽（BNP）和肌钙蛋白存在显著差异（P<0.05或P<0.01）；此外，不同组患者运动负荷存在不同，Zn水平更高的患者运动负荷更好；1年随访后结果随访发现Zn水平的降低伴随更高的心源性死亡及死亡的风险；Cox比例风险回归模型发现Zn可以作为预测因子判断CHF患者心源性死亡，但同时收到其他因素如患者并发症或LDL水平的影响。 结论 CHF患者血清Zn水平的下降意味着患者死亡风险更高，并且运动负荷降低。      

Elevated plasma beta-endorphin levels in patients with congestive heart failure

Recent experimental studies show that the opioid system is important to the pathophysiology of cardiovascular impairment in congestive heart failure. Plasma beta-endorphin levels were measured in 37 patients with congestive heart failure and compared with those of 21 age- and gender-matched normal subjects. The relation of plasma beta-endorphin levels and cardiac function at rest and exercise capacity was assessed in 17 of the patients with dilated cardiomyopathy. Exercise capacity was determined by symptom-limited maximal treadmill exercise with expired gas analysis. Plasma beta-endorphin levels were elevated and correlated with the patients' New York Heart Association functional cardiac status (control: 14.0 +/- 4.4 pg/ml; class II: 17.9 +/- 3.6 pg/ml; class III: 28.3 +/- 8.8 pg/ml; class IV: 46.7 +/- 14.6 pg/ml, mean +/- SD). No relation was found between plasma beta-endorphin levels and left ventricular systolic performance as assessed by M-mode and Doppler echocardiography. Plasma beta-endorphin levels were negatively correlated with cardiac output determined by Doppler echocardiography and positively correlated with systemic vascular resistance (r = -0.733, r = 0.747, respectively, both p less than 0.001), but not correlated with calf blood flow as measured by a plethysmography. A good correlation was found between plasma beta-endorphin levels at rest and exercise capacity. The correlations with peak oxygen consumption, anaerobic threshold, and peak rate-pressure product were r = -0.721, -0.672, and -0.674, respectively (p less than 0.01). The data show that plasma beta-endorphin levels are elevated in patients with congestive heart failure and reflect, to some degree, the severity of the disease.     

Development of congestive heart failure after treatment with metoprolol in acute myocardial infarction.

In a double blind study of metoprolol in the treatment of suspected acute myocardial infarction 698 patients (study group) received metoprolol and 697 a placebo (control group). Metoprolol was given in an intravenous dose of 15 mg as soon as possible after admission to hospital followed by 50 g by mouth four times a day for two days and thereafter 100 mg twice a day for three months. A placebo was similarly given. Congestive heart failure occurred in a similar percentage of patients in both the study (27%) and the control groups (30%). Its severity was estimated by calculating the total dose of frusemide given during the first four days in hospital. Less frusemide was given to patients treated with metoprolol compared with those given a placebo in the total series. An appreciably lower total dose of frusemide was given to patients included in the trial less than or equal to 12 hours after the onset of pain and treated with metoprolol compared with a placebo, while no difference was seen among patients treated later. The initial heart rate, systolic blood pressure, and infarct site affected the results.     

Vasodilator therapy for acute myocardial infarction and chronic congestive heart failure

Vasodilator therapy is useful adjunctive therapy in the management of both acute and chronic heart failure. Arteriolar dilators, such as hydralazine, increase cardiac output by decreasing the elevated peripheral vascular resistance that occurs in heart failure. Venodilators, such as nitrates, decrease ventricular filling pressures by redistributing blood so that more is pooled in peripheral veins. Vasodilators that produce both effects (nitro-prusside, prazosin, captopril, for example) are usually helpful in short-term improvement of hemodynamics. Long-term treatment with nonparenteral vasodilators often reduces symptoms and increases exercise tolerance, although there is inconclusive evidence regarding the effects of these agents on mortality. In acute myocardial infarction, intravenous vasodilators frequently improve cardiac performance. Evidence regarding their beneficial effects on infarct size and immediate mortality is encouraging but inconclusive. There is little evidence that they prolong life in patients who survive cardiogenic shock and leave the hospital. Thus, vasodilators can improve hemodynamics and lessen symptoms, but more evidence is needed regarding their long-term effects on survival.     

血浆同型半胱氨酸水平与心肌梗死的相关性

目的探讨血浆同型半胱氨酸(Hcy)水平与心肌梗死的关系。方法我院2012年1月至2013年12月间收治的40例心肌梗死患者作为心肌梗死组,选取同期行健康体检的正常人40例作为非心肌梗死组,比较两组血浆Hcy水平及治疗后心肌梗死组患者Hcy水平,分析心肌梗死危险因素。结果心肌梗死组患者血浆Hcy水平明显高于非心肌梗死组,治疗后,心肌梗死组Hcy水平较治疗前有明显下降,差异均具有统计学意义(P0.05);血浆Hcy高表达为心肌梗死独立危险因素。结论血浆Hcy水平与心肌梗死有一定的相关性,高Hcy为心肌梗死的独立危险因素。     

急性心肌梗死患者血浆脑尿钠肽与心功能的相关性

目的:探讨急性心肌梗死(AMI)患者血浆脑钠尿肽(BNP)与左心室射血分数(LVEF)、左心室舒张末容积(LVEDV)、Killip分级及心肌梗死部位的关系,评价BNP对AMI患者心功能和危险分层的预测价值。方法:检测120例AMI患者和120例对照组血浆BNP水平,同时行心脏彩色多普勒检测LVEF、LVEDV,比较AMI组与对照组以及不同LVEF、Killip分级和不同梗死部位亚组间的血浆BNP水平差异。结果:与对照组相比,AMI组BNP和LVEDV显著升高,LVEF显著降低(均P<0.01)。与LVEF>50%组比较,LVEF<40%组BNP、LVEDV显著升高(P<0.05);与Killip I、II级比较,Killip III、IV级组BNP显著升高(P<0.05),Killip IV级组LVEDV显著增大(P<0.05)。与下壁心肌梗死患者相比,下后壁、前壁梗死患者BNP显著升高(P<0.05)。BNP与Killip分级成正相关(r=0.97,P<0.05),与LVEF成负相关(r=-0.33,P<0.05)。结论:AMI患者血浆BNP显著增高,尤以LVEF<40%、Killip IV级、前壁心肌梗死者为甚。     

Association between plasma endothelin-1 levels and Cheyne-Stokes respiration in patients with congestive heart failure

STUDY OBJECTIVES: Elevated plasma endothelin-1 (ET-1) levels have been reported in association with hypoxia and congestive heart failure (CHF). Furthermore, Cheyne-Stokes respiration-central sleep apnea (CSR-CSA) has been found to correlate with the degree of pulmonary hypertension and the severity of CHF; however, the association between ET-1 levels and CSR-CSA has not been investigated previously. SETTING: Veterans Affairs Medical Center. INTERVENTIONS: We studied 46 consecutive patients with CHF (left ventricular function < or = 40%) who underwent right-heart catheterization and overnight polysomnography. Thirty-nine patients completed the study. Sixteen patients (41%) had CSR-CSA, 5 patients (13%) had obstructive apnea, and 18 patients (46%) had no sleep-disordered breathing. Circulating plasma ET-1 levels were assayed in patients with CSR-CSA and in patients with no sleep-disordered breathing using commercially available enzyme-linked immunosorbent assay kits. RESULTS: ET-1 levels were significantly elevated in patients with CSR-CSA (mean +/- SD, 5.4 +/- 1.3 pg/mL) compared to those without central apnea (3.9 +/- 1.1 pg/mL; p < 0.01), and correlated with mean pulmonary artery pressure (r = 0.66, p < 0.01), pulmonary capillary wedge pressure (r = 0.56, p < 0.03), and central apnea frequency (r = 0.66, p < 0.01). In multivariate analysis, the severity of CSR-CSA was the only variable independently associated with plasma ET-1. CONCLUSIONS: We conclude that elevated plasma ET-1 levels are linked to the severity of CSR-CSA. Whether ET-1 represents an important pathogenic factor in CSR-CSA or marker of its occurrence requires further evaluation.     

Characteristics and prognosis of patients with acute myocardial infarction in relation to occurrence of congestive heart failure

Congestive heart failure is one of the major symptoms accompanyingacute myocardial infarction (AMI). The study aimed to describethe occurrence, characteristics and prognosis of congestiveheart failure in AMI and to compare post-MI patients with andwithout congestive heart failure. The methods used includedbaseline characteristics, initial symptoms, electrocardiogram(ECG), mortality during hospitalization and one year follow-upin consecutive patients with AMI admitted to Sahlgrenska Hospital,Göteborg, Sweden. Congestive heart failure was observed in 51% of the cases. Patientswith congestive heart failure were older, more frequently hada history of previous cardiovascular disease, and, less frequentlyhad chest pain on admission to hospital. They had a higher occurrenceof life-threatening ventricular arrhythmias during initial hospitalization,and their mortality during one year follow-up was 39% as comparedto 17% in patients without congestive heart failure (P<0.001).This difference remained significant when correcting for differencesat baseline. Patients with severe congestive heart failure hada one year mortality of 47% vs 31% in patients with moderatecongestive heart failure (P<0.01). Signs and symptoms of congestive heart failure occur in everysecond patient admitted to hospital due to AMI, and indicatea bad prognosis, which is directly related to the severity ofcongestive heart failure.     

Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction.

For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.     

急性心肌梗死患者Killip心功能分级与血浆促心肌素-1浓度变化的关系

目的 探讨急性心肌梗死(acute myocardial infarction,AMI)患者Killip功能分级与血浆促心肌素-1(cardiotrophin-1,CT-1)浓度变化的关系.方法 选择2008年4月～2008年10月于海南医学院附属医院心血管内科住院的29例AMI患者为研究对象,根据入院时Kiflip分级分组,其中Killip Ⅰ组11例,年龄(64±11)岁;KillipⅡ组10例,年龄(67±15)岁;KifiipⅢ组8例,年龄(68±15)岁.另外,选择20例排除CT-1增高疾病的患者为正常对照组,年龄(63±8)岁.收集入选者血清肌酸激酶同工酶、血清肌钙蛋白浓度,并用酶联免疫吸附测定方法 测定血浆CT-1浓度,所得数据用SPSS软件包进行统计学分析.结果 方差分析显示4组心肌肌钙蛋白Ⅰ浓度、血清肌酸激酶同工酶浓度、血浆CT-1浓度比较,差异有统计学意义(F=3.709,P<0.05;F=3.617,P<0.05;F=18.343,P<0.05).KillipⅢ组血浆CT-1浓度高于Killip Ⅰ组及Killip Ⅱ(613.25±84.85)pg/mL vs.(299.36±139.56)pg/mL,P<0.05]; [(613.25±84.85)pg/mL vs.(394.11±67.89)pg/mL,P<0.05].Pearson相关分析显示,AMI患者Killip分级与血浆CT-1浓度呈正相关(r2=0.77,P<0.01),与肌酸激酶同工酶峰值呈正相关(r2=0.44,P<0.05),与心肌肌钙蛋白峰值呈正相关(r2=0.39,P<0.05).AMI患者血浆CT-1浓度与心肌肌钙蛋白峰值呈正相关(r2=0.555,P<0.01),与肌酸激酶同工酶峰值呈正相关(r2=0.614,P<0.01).结论 血浆CT-1浓度在AMI患者中明显升高,其浓度与Killip心功能分级相关.