酒精与中风

众所周知,酗酒可导致急性和慢性脑损害,最近有人提出酗酒的另一危险是引起中风。本文回顾了酒精与脑血管疾病相关连的依据。心血管作用酒精对心血管系统有明显的作用,急性饮酒可使心率及心输出量增加,左心室收缩功能下降,收缩压升高,脉压加大,心脏前负荷及外周血管阻力下降,皮肤血管扩张而内脏血管收缩,心肌耗氧量增加,因此冠脉血流增加。适量饮酒可降低冠心病的死亡率,而大量饮酒则可导致某些心脏并发症,后者增加了缺血性脑卒中的危险。并发症之一是所谓“假日心脏”综合征(“holiday heart”syndrome)。Ettinger 等发现     

慢性饮酒对大鼠主动脉血管反应性的影响及牛磺酸的干预作用

目的探讨慢性饮酒对大鼠血管反应性的影响及牛磺酸的干预作用。方法采用离体血管张力实验方法,观察吡那地尔(Pinacidil)和氨力农(Amrinone)对10μmol/L去甲肾上腺素(NE)和60mmol/LKCl引起的各组大鼠主动脉的收缩影响。实验末通过泰盟尾动脉清醒测压仪分别测定各组大鼠收缩压(SBP)及舒张压(DBP)。结果10-6mol/LPinacidil对NE预收缩的牛磺酸组大鼠主动脉的舒张率与饮酒组相比升高(P0.05);10-8mol/L、10-7mol/LPinacidil对KCl预收缩的牛磺酸组大鼠主动脉的舒张率与饮酒组相比均升高(P0.05);10-8mol/L、10-7mol/L及10-6mol/LAmrinone对NE预收缩的牛磺酸组大鼠主动脉舒张率与饮酒组相比均升高(P0.05);和对照组比较,饮酒组大鼠的SBP和DBP均升高;和饮酒组比较,牛磺酸组大鼠的SBP和DBP均降低(P0.05)。结论慢性饮酒大鼠主动脉对舒血管物质Pinacidil和Amrinone血管舒张反应变化不明显,但可引起大鼠血压升高;牛磺酸可增强慢性饮酒大鼠主动脉对Pinacidil和Amrinone的血管舒张作用,降低升高的血压。     

硝普钠在肺心病顽固性心力衰竭并高血压中的应用

目的　观察硝普钠伍用多巴胺治疗慢性肺心病顽固性心力衰竭并高血压的疗效。方法　除继续采用有效抗生素、吸氧、保持呼吸道通畅等对症治疗外 ,予硝普钠 5 0 m g、多巴胺 2 0 mg加入 5 %葡萄糖注射液 5 0 0 ml中避光静脉滴注 ,疗程 3 d。结果　显效 2 9例 (72 .5 % ) ,有效 11例 (2 7.5 % ) ,总有效率达 10 0 % ;用药 3 0 m in后心率、呼吸频率、血压即有明显改善 (P<0 .0 5 ,P<0 .0 1) ,治疗后改善更为显著 (P<0 .0 1) ;心率血压乘积明显下降 (P<0 .0 1) ,心肌耗氧量降低 ;随着疗程的进行 ,左心室射血分数 (L VEF)、左心室短轴缩短率 (FS)及舒张早期最大充盈速度(E)与舒张晚期最大充盈速度 (A)的比值 (E/ A)明显增加 ,治疗后增加显著 (P<0 .0 1) ;血浆 NO增加 (P<0 .0 5 ) ,第一秒用力呼气量 (FEV1 )、动脉血氧分压 (Pa O2 )和动脉血二氧化碳分压 (Pa CO2 )均较治疗前有所改善 (P<0 .0 5 ,P<0 .0 1) ;治疗后共有 14例 (43 .8% )原有心律失常消失。结论　硝普钠与多巴胺联合治疗肺心病顽固性心力衰竭并高血压有良好效果     

肾交感神经去除术对心力衰竭犬心功能的影响

目的:研究肾交感神经去除术(RDN)对心力衰竭(HF)犬心功能的影响。方法:选择实验犬40只,随机均分为RDN组(接受双肾动脉射频消融)及模型组(仅予股动脉穿刺)。40只犬均安置心脏起搏器,用快速右室起搏的方法制造犬心衰动物模型。观察每只犬射频消融/假手术前,建模4周后的心、肾功能指标,BNP以及交感活性指标水平,并进行组间比较。结果:术后4周,与模型组比较,RDN组的肾上腺素(E)[(362.69±42.54)ng/ml比(290.36±42.32)ng/ml],肾素(R)[(305.46±39.68)ng/ml比(230.04±32.80)ng/ml],醛固酮(AD)[(408.00±38.56)ng/ml比(246.00±48.37)ng/ml],血管紧张素Ⅱ(ATⅡ)[(280.00±48.08)pg/ml比(172.00±25.04)pg/ml]和去甲肾上腺素(NE)[(425.65±50.54)ng/ml比(316.76±46.29)ng/ml]水平均显著降低(P均0.05);与模型组比较,RDN组HR,呼吸频率(RR)和BNP显著降低(P均0.05);SBP、LVEF、CO、CI、左心室压力最大上升速率(+dp/dtmax)、左心室压力最大下降速率(-dp/dtmax)和左室收缩末压(LVESP)显著升高,左室收缩末期内径(LVESd),左室舒张末期内径(LVEDd)和左室舒张末压(LVEDP)显著降低,P均0.05;结论:RDN降低心衰犬的肾交感活性,改善心功能,抑制右室起搏所致心肌重构,疗效显著。     

糖尿病树鼩血栓性脑缺血时心脏血流动力学及心肌超微结构的变化

目的观察实验性糖尿病树鼩在血栓性局部脑缺血时心脏血流动力学及心肌超微结构的变化。方法链脲佐菌素(STZ)55mg/kg空腹腹腔注射制备糖尿病树鼩模型,一周后通过光化学反应诱导局部血栓性脑缺血。将树鼩随机分为糖尿病组,脑缺血组,糖尿病加脑缺血组,并设假手术对照组,每组8只,用多导生理仪观察左心室内压(LVSP)、左心室舒张末压(LVEDP),左心室收缩与舒张瞬间变化最大速率(±dp/dtmax),收缩动脉压(SAP),舒张动脉压(DAP)及心率(HR)。并取左心室心肌组织,行透射电镜观察心肌超微结构变化。结果 与假手术对照组相比,脑缺血组LVSP、+dp/dtmax下降(P<0.05),-dp/dtmax明显下降(P<0.01),LVEDP升高(P<0.05);糖尿病组-dp/dtmax下降(P<0.05),LVEDP明显升高(P<0.01)。与脑缺血组相比,糖尿病加脑缺血组LVSP、+dp/dtmax降(P<0.05),-dp/dtmax明显下降(P<0.01),LVEDP升高(P<0.05)。脑缺血组和糖尿病组心肌超微结构观察显示:心肌肌原纤维间水肿,一些肌原纤维可见收缩小带形成,部份线粒体固缩,部份线粒体肿胀。糖尿病加脑缺血组树鼩可见:大部分线粒体固缩,部分线粒体肿胀、嵴溶解,心肌纤维较多收缩带形成,间质充血水肿,毛细血管内皮细胞见较多空泡。结论树鼩血栓性脑缺血时伴有心脏血流动力学及心肌超微结构的异常,糖尿病急     

黄芪皂苷注射液对急性心衰犬心功能和血流动力学的影响

目的 观察黄芪皂苷注射液对实验性心衰犬心功能和血流动力学的影响.方法 采用β受体阻滞剂心得安诱发麻醉犬在体急性心衰模型,静脉注射黄芪皂苷注射液,同时测定心输出量(CO)、心脏指数(CI)、左心室收缩压(LVSP )、左室舒张末压(LVEDP)、收缩压最大上升速率(+dp/dtmax)及舒张压最大下降速率(-dp/dtmax)等心功能指标.结果 黄芪皂苷注射液对心衰犬CO 、CI 及LVSP、+dp/dtmax、-dp/dtmax均有明显的增加作用.结论 黄芪皂苷注射液具有增加col、增强心肌收缩力和改善心脏舒缩功能的作用.将其研制成强心和改善心功能药物具有良好的应用前景.     

急性心肌梗死后血浆神经内分泌激素水平与心功能的关系

目的　通过测定急性心肌梗死 (AMI)患者血浆中神经内分泌激素水平 ,探讨AMI后神经内分泌系统的激活与心功能的关系。方法　 5 7例AMI患者 ,依据左心室射血分数 (LVEF)将AMI患者分为A、B两组 ,A组 :31例 ,LVEF≥5 0 % ;B组 :2 6例 ,LVEF <5 0 %。另选 2 0例健康人作为正常对照组。分别采血检测血浆肾素活性 (PRA)、血管紧张素Ⅱ (AngⅡ )浓度、血浆醛固酮 (ALD)浓度、血浆去甲肾上腺素 (NE)和肾上腺素 (E)浓度。结果　AMI后心功能较差的B组患者血浆PRA、AngⅡ、NE、E水平较正常对照组升高 ,其中尤以NE升高最为显著 (P <0 .0 0 1)。结论　AMI后心功能减退会进一步增强神经内分泌系统的活性。     

电脑非线性阻抗法测定高血压患者心功能及其相关性分析

以电脑非线性阻抗法测定了54例高血压患者的左心室泵血功能,左心室收缩功能、舒张功能,以及心脏前、后负荷,与60例健康人比较,并将反映心脏前、后负荷的指标与左心室泵血功能及收缩和舒张功能进行线性相关分析,结果发现,左心室泵血功能显著下降(P<0.05～0.01),左心室收缩功能无显著改变,而舒张功能显著下降(P<0.01),心脏前负荷与泵功能及收缩功能显著相关(P<0.01),心脏后负荷与泵功能及舒张功能显著负相关(P<0.01),认为高血压病患者后负荷升高,可导致左心室泵功能及舒张功能障碍,是左心室受损的早期表现。     

糖尿病患者左心室结构及功能的超声评价

目的　观察 2型糖尿病患者心脏结构、重量、功能的变化情况 ,作出及时的诊断和防治。方法　采用 HPSONOS5 5 0 0彩色多普勒超声心动图对 76例 2型糖尿病患者和 60例正常对照组测定左心室收缩、舒张功能、左心室重量、左心房左心室内径。结果　 2型糖尿病患者的左心室结构改变、心肌重量增加 ,比舒张功能障碍较早出现 ,与正常对照组比较有显著意义 ( P<0 .0 0 1) ;随病程延长 ,病情加重 ,左心室左心房明显扩大 ,左心室舒张功能出现“假性正常化”,而收缩功能出现障碍 ,与正常对照组比较有显著意义 ( P<0 .0 0 1)。结论　彩色多普勒超声心动图对2型糖尿病患者的心脏结构、功能、重量及临床疗效判断具有重要价值。     

非洛地平控释片的降血压疗效及对左心室功能的影响

目的　随访观察非洛地平控释片 (波依定 )的降血压疗效和对左心室功能的影响。方法　应用波依定治疗原发性高血压 92例 ,硝苯地平作对照组 ,随访治疗 3年 ,治疗前后作 2 4h动态血压监测和彩色多普勒超声心动图评价临床疗效 ,治疗中 ,作常规血压观察。结果　治疗后治疗组 2 4h、白昼和夜间平均收缩压、平均舒张压水平较治疗前和硝苯地平组显著下降 (P<0 .0 5 ) ,昼夜降血压幅度相似 ;而对照组 2 4h血压波动较大 ,夜间降压不显著。波依定降压的谷 /峰比值 ,收缩压为 72 .3 % ,舒张压为 81.5 %。治疗前后彩色多普勒超声心动图检测显示 ,治疗组能够改善左心室收缩功能和舒张功能 ,且室间隔、左心室舒张末期内径、左心室后壁厚度无明显变化 ,而对照组对左心室收缩功能和舒张功能有降低的趋势 (P<0 .0 5 ) ,且室间隔、左心室舒张末期内径、左心室后壁厚度明显增大 (P<0 .0 5 )。波依定组不良反应较硝苯地平组轻 (P<0 .0 1)。结论　波依定在高血压病治疗中较短效制剂为优 ,并能改善左心室收缩和舒张功能和预防左心室肥厚发生的可能。     

心肌梗死大鼠左心室收缩与舒张功能的改变及其影响因素

目的 探讨心肌梗死大鼠左心室收缩和舒张功能的改变、以及心室重构对心室舒缩功能的影响.材料和方法结扎Wistar大鼠左冠状动脉、制成心肌梗死模型,6周后测定左室心肌力学指标,心肌胶原含量、血浆及心肌的血管紧张素Ⅱ(Aug Ⅱ)浓度.结果 心肌梗死组与对照组比较,LVPSP、+dp/dt_(max)、dp/dt_(max)绝对值及V_(max)明显降低(P<0.01),LVEDP增加(P<0.01),T值延长(P<0.01),MAP无差异.心肌梗死组与对照组比较、心肌羟脯氨酸和心肌胶原含量明显增高(P均0.01),心肌AngⅡ含量明显升高(P<0.01)、血浆AngⅡ浓度无显著差异.结论 心肌梗死后左室收缩与舒张　功能明显降低,同时出现心肌细胞的肥大和纤维细胞的增生以及间质纤维化、后者可进一步导致和加重心脏泵血功能的异常.     

高血压病患者动态血压与左心功能相关关系的研究

目的观察收缩压、舒张压分别对左室收缩及舒张功能的不同影响。方法应用诊所血压、２４小时动态血压监测及超声心动图，观察３８例Ⅰ、Ⅱ期高血压病患者血压与左室心肌质量、左室收缩及舒张功能的相关关系。结果２４小时及白天平均收缩压及诊所收缩压均与舒张早期充盈峰值流速（ＥＰＦＶ）呈负相关（Ｐ值均＜００５），２４小时、白天及夜间平均舒张压均与年龄呈负相关（Ｐ值均＜０．０５），与舒张功能各参数之间无相关关系，诊所收缩压与年龄、心房收缩期充盈峰值流速（ＡＰＦＶ）呈正相关（Ｐ＜０．００１及０．０５），夜间平均收缩压及诊所收缩压与左室心肌质量指数呈正相关（Ｐ＜０．０１及０．０５）。而２４小时平均收缩压、白天平均收缩压、２４小时平均舒张压、白天及夜间平均舒张压则均与左室心肌质量指数无明显相关关系。结论２４小时平均收缩压是影响左室舒张功能的重要因素之一，２４小时平均舒张压与左室舒张功能无相关关系。夜间平均收缩压增高是导致左心室肥厚的重要因素之一。随年龄增长，收缩压增高，舒张压下降     

长期低氧暴露对健康青年男性心脏结构和功能的影响

目的 通过对长期低氧暴露下健康青年男性心脏彩超基础数据的分析比较,揭示低氧暴露下心脏结构和功能的变化特征,探索防治高原肺动脉高压及慢性高原性心脏病的临床意义。 方法 纳入37名健康青年男性,采用低氧暴露前后自身对照的方法,利用心脏彩超测量左心房内径（LAD）、右心房内径（RAD）、左心室内径（LVD）、主动脉内径（AOD）、室间隔厚度（VST）、左室后壁厚度（LVPWT）、肺动脉内径（PAD）、右室流出道内径（RVOT）、左室短轴缩短率（LVFS）、左心室射血分数（LVEF）、左室舒张早期充盈流速（LVEDFV）、左室舒张晚期充盈流速（LVLDFV）、左室舒张早期/晚期充盈流速比（E/A）和肺动脉收缩压(PASP),进行对比分析。 结果 低氧暴露后,HR显著升高（P<0.01）,LVEF、LVFS及E/A均显著降低(均P<0.01);低氧暴露对心脏结构和功能有显著影响,低氧暴露后LAD、LVD、AOD、VST、LVPWT均显著降低（均P<0.01）,RAD（P<0.05）、PAD、RVOT（P<0.01）均显著升高。低氧暴露后,56.8%的受试对象肺动脉收缩压明显增高。PAH-组在低氧暴露后LVEDFV及E/A显著降低(均P<0.01),LVLDFV显著升高(均P<0.01);而PAH+组在低氧暴露后LVEF、LVFS、LVEDFV及E/A显著降低(均P<0.01),在低氧暴露前,PAH+组受试对象LVFS和LVEF均显著高于PAH-组(均P<0.05);PAH+组△LVFS和△LVEF的变化幅度均高于PAH-组（均P<0.01）。 结论 长期高原低氧暴露可引起肺动脉压升高以及心脏结构和功能发生显著变化;低氧暴露前LVFS和LVEF基础水平较高者或更易成为PAH易感人群。     

Left ventricular dysfunction in hypertensive patients with Type 2 diabetes mellitus.

AIMS: To characterize left ventricular function in hypertensive patients with Type 2 diabetes and normal ejection fraction, and to relate these findings to pathogenic factors and clinical risk markers. METHODS: We examined 70 hypertensive patients with Type 2 diabetes mellitus with ejection fraction > 0.55 and fractional shortening > 0.25, all without any cardiac symptoms. Thirty-five non-diabetic subjects served as control subjects. Left ventricular longitudinal function was examined by tissue Doppler derived myocardial strain rate and peak systolic velocities. RESULTS: Hypertensive patients with diabetes had a significantly higher systolic strain rate (-1.1 +/- 0.3 s(-1) vs. -1.6 +/- 0.3 s(-1), P < 0.001) and lower systolic peak velocities (3.3 +/- 1.0 vs. 5.6 +/- 1.0 cm/s, P < 0.001) compared with control subjects. Myocardial systolic strain rate correlated significantly to left ventricular mass (r = 0.40, P < 0.01) and to both HbA1c (r = 0.43, P < 0.01), and fructosamine (r = 0.40, P < 0.01), but was not related to serum levels of carboxymethyllysine, albuminuria, blood pressure (dipping/non-dipping), or oral hypoglycaemic therapy. Patients with diastolic dysfunction had significantly higher levels of urine albumin [21.0 (5-2500) mg/l, vs. 9.5 (1-360), P < 0.01], heart rate (78 +/- 13 vs. 67 +/- 10 b.p.m., P < 0.005), and seated diastolic blood pressure (85 +/- 6 vs. 81 +/- 7 mmHg, P < 0.05) and non-dipping diastolic blood pressure was more frequent. CONCLUSIONS: Long axis left ventricular systolic function was significantly decreased in hypertensive patients with Type 2 diabetes mellitus, and is associated with hyperglycaemia and left ventricular hypertrophy. Diastolic dysfunction was closely related to increased diastolic blood pressure, non-dipping and increased urinary albumin excretion.     

Sympathetic (alpha-beta) or calcium channel blockade for hypertensive myocardial infarction? A haemodynamic comparison of labetalol and nifedipine

The haemodynamic impact of alpha- and beta-adrenoceptor blockade (labetalol) was compared with that of slow-calcium channel blockade (nifedipine) in 32 patients with sustained elevation of systemic arterial pressure (systolic blood pressure greater than 160; diastolic blood pressure greater than 95 mmHg) following a recent myocardial infarction (6-22 h). Patients with normal (pulmonary artery occluded pressure; (PAOP less than 18 mmHg; n = 16) or impaired (PAOP greater than 18 mmHg; n = 16) left ventricular function were randomized to labetalol (1 mg/kg i.v. 15 min) or nifedipine (20 mg sublingually) and haemodynamic profile was measured over 2 h. Both drugs equally reduced mean systemic arterial pressure (P less than 0.01 versus pretreatment control), and presumably left ventricular afterload; however, the heart rate (P less than 0.01) and cardiac index (P less than 0.01) increased after nifedipine, contrasting with reductions in both variables following labetalol (P less than 0.01). The elevated left ventricular filling pressure was reduced by both labetalol (P less than 0.05) and nifedipine (P less than 0.01) but the reduction was greater following nifedipine (-2 mmHg versus -5 mmHg, P less than 0.05). Thus both compounds were equally effective hypotensive agents. Labetalol consistently reduced cardiac stroke work and double product, important determinants of myocardial oxygen requirements; however, nifedipine afforded some improvement in cardiac performance in patients with left ventricular dysfunction.     

Arterial pressure, left ventricular mass, and aldosterone in essential hypertension

The purpose of the present study was to evaluate the relationship of aldosterone to blood pressure and left ventricular size in black American (n=109) and white French Canadian (n=73) patients with essential hypertension. Measurements were obtained with patients off antihypertensive medications and included 24-hour blood pressure monitoring, plasma renin activity and aldosterone, and an echocardiogram. Compared with the French Canadians, the black Americans had higher body mass indexes, higher systolic blood pressures, attenuated nighttime reduction of blood pressure, and lower serum potassium concentrations (P:<0.01 for each). Left ventricular mass index, posterior wall thickness, interventricular septal thickness, and relative wall thickness were also greater (P:<0.01 for each) in the black American patients. Supine and standing plasma renin activity was lower (P:<0.01 and P:<0.05, respectively) in the black Americans, whereas supine plasma aldosterone concentrations did not differ, and standing plasma aldosterone was greater (P:<0.05) in the black Americans (9.2+/-0.7 ng/dL) than in the French Canadians (7.3+/-0.6 ng/dL). In the black Americans, supine plasma aldosterone was positively correlated with nighttime systolic (r=0.30; P:<0.01) and diastolic (r=0.39; P:<0.001) blood pressures and inversely correlated with the nocturnal decline of systolic (r=-0.29; P:<0.01) and diastolic (r=-0.37; P:<0.001) blood pressures. In the black Americans, standing plasma aldosterone was positively correlated with left ventricular mass index (r=0.36; P:<0.001), posterior wall thickness (r=0.33; P:<0.01), and interventricular septal thickness (r=0.26; P:<0.05). When the black American patients were divided into obese and nonobese groups, significant correlations between plasma aldosterone and both blood pressure and cardiac mass were observed only in the obese. In the French Canadians, overall, plasma aldosterone did not correlate with either blood pressure or any measures of heart size. However, among obese French Canadians, supine plasma aldosterone correlated with nighttime diastolic (r=0.53, P:<0.02) and systolic (r=0.44, P:<0.01) blood pressures but not with cardiac mass. These results are consistent with the hypothesis that aldosterone contributes to elevated arterial pressure in obese black American and obese white French Canadian patients with essential hypertension and to the attenuated nocturnal decline of blood pressure and left ventricular hypertrophy in obese, hypertensive black Americans.     

Comparison between office and ambulatory blood pressure in young and elderly subjects with isolated systolic hypertension

BACKGROUND: It has been claimed that isolated systolic hypertension (ISH) in the elderly is not a sustained condition but a short-lasting increase in office systolic blood pressure magnified by arterial stiffness. DESIGN: Office and ambulatory blood pressures werecompared at baseline and after 3 months of observation of young and elderly subjects with ISH. METHODS: The study was carried out in 39 young (mean age 27.1+/-9.8 years) and 37 elderly patients (mean age 72.5+/-5.7 years). Office blood pressure was defined as the mean of six readings. All subjects underwent two non-invasive 24 h blood pressure monitorings performed 3 months apart and echocardiography (n = 50). RESULTS: The difference between office and mean 24 h systolic/diastolic blood pressure was 27.9/8.2 mmHg in the young and 18.9/6.9 mmHg in the elderly patients (P < 0.01 for systolic blood pressure). Twenty-four-hour (P < 0.001), daytime (P = 0.001) and night-time (P < 0.001) systolic blood pressures were higher in the elderly and the difference between daytime and night-time systolic blood pressure was greater in the young (P < 0.05). Office and ambulatory heart rates were significantly higher in the young subjects. The elderly patients showed a greater left ventricular wall thickness ( P = 0.005 for posterior wall; P < 0.005 for septum), relative wall thickness (P = 0.01) and left ventricular mass index (P = 0.001) and impaired left ventricular filling rate ( P = 0.05), whereas systolic performance and stroke volume were no different in the two groups. Due to the higher heart rate, cardiac output was greater in the young (P = 0.03). CONCLUSION: These data show that larger differences between office and ambulatory systolic blood pressure are not unique to elderly patients with ISH. Increased ambulatory blood pressure levels and a decreased nocturnal blood pressure fall were associated with left ventricular structural and functional abnormalities in the elderly subjects.     

Effects of sublingually administered nifedipine on left ventricular isovolumic relaxation, diastolic filling, and distensibility in patients with chronic coronary artery disease.

The acute effects of nifedipine (20 mg) on left ventricular diastolic function were investigated in 16 patients with chronic coronary artery disease by measuring left ventricular pressure with a manometer-tipped catheter and by measuring volume with cineangiography. Heart rates were maintained by right atrial pacing. Left ventricular peak systolic pressure (-15%; p less than 0.01 vs control) decreased significantly. With afterload reduction, left ventricular ejection fraction (+11%; p less than 0.01) increased. There was no significant change in left ventricular end-diastolic pressure. The diastolic peak filling rate of left ventricular volume significantly increased (+36%; p less than 0.05), whereas the time from end-systole to the peak filling rate remained unchanged. Administration of nifedipine did not improve left ventricular relaxation as assessed by the isovolumic pressure decay. There was also no significant change in the left ventricular diastolic pressure-volume relationship. We conclude that nifedipine improves left ventricular systolic function with afterload reduction but has little or no effect on left ventricular diastolic properties in patients with chronic coronary artery disease.     

Effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation in man.

The effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation were investigated in 13 patients in whom systemic hypertension developed following coronary artery bypass surgery. Pulmonary vascular resistance was decreased by the inhibitor, from 128 ± 19 to 92 ± 20 dynes sec cm^?5 (or by 30 ± 7 per cent; P < 0.005), and this resulted in a decrease in mean pulmonary artery pressure from 17 ± 1 to 13 ± 1 mm Hg (or by 23 ± 3 per cent, P < 0.005). Consequently, right ventricular work was decreased by the inhibitor by 30 per cent (P < 0.01), despite an increase in cardiac output (increase in stroke volume) by 16 ± 6 per cent (P < 01). This increase occurred despite a 13 ± 3 per cent decrease in right ventricular filling pressure. The changes in pulmonary vascular resistance correlated with the pretreatment plasma renin activity (r = 0.74, P < 0.01), as did the decrease in mean pulmonary artery pressure (R = 0.82, P < 0.001), but neither change was related to the decrease in left ventricular filling pressure nor to changes in cardiac output or mean arterial pressure.These results indicate that blockade of the formation of angiotensin II by the converting enzyme inhibitor results in reductions in pulmonary vascular resistance and pulmonary artery pressure which are unrelated to alterations in left ventricular function. Thus, angiotensin inhibition may have therapeutic value in various clinical states characterized by pulmonary hypertension—especially if renin levels are high.     

The effect of caffeine on exercise tolerance and left ventricular function in patients with coronary artery disease

STUDY OBJECTIVE: To determine whether acute oral caffeine ingestion by patients with coronary artery disease results in decreased treadmill exercise performance or deterioration of echocardiographic measures of systolic or diastolic left ventricular function. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Referral-based cardiovascular exercise laboratory at an urban teaching hospital. PATIENTS: Thirteen volunteers with clinically stable coronary artery disease who had exercise tests after a 2-week caffeine-free washout period. Patients continued treatment with standard antianginal medications during the study period. INTERVENTIONS: Maximal exercise treadmill testing and exercise echocardiography were done at baseline, after acute ingestion of a placebo beverage (97% caffeine-free coffee), or after drinking an identical beverage containing 250 mg of caffeine sodium benzoate. MEASUREMENTS AND MAIN RESULTS: Acute ingestion of caffeine produced a serum level of 4.50 +/- 0.16 micrograms/mL, but had no effect on resting supine heart rate, blood pressure, left ventricular fractional shortening, posterior left ventricular wall thinning or peak rates of increase in left ventricular diastolic dimension. Despite a small increase in peak systolic blood pressure during exercise (baseline, 153 +/- 8; placebo, 154 +/- 8; caffeine, 161 +/- 7 mm Hg; P less than 0.05), exercise duration, time to onset of angina, and time to 0.1 mV ST depression did not differ after ingestion of placebo or caffeine. Rate-pressure product at onset of angina and onset of 0.1 mV of ST depression were also unchanged. In response to exercise, echocardiographic measures of left ventricular systolic and diastolic function were unchanged after caffeine compared with placebo ingestion. CONCLUSIONS: These data suggest that patients with exercise-induced ischemia who are receiving appropriate antianginal therapy tolerate the caffeine-equivalent of three cups of coffee without detrimental effect on intensity of ischemia, myocardial function, or exercise duration.