扩张型心肌病冠状动脉血流储备功能的超声研究

目的 应用多平面经食管多普勒超声心动图(TEE)潘生丁负荷试验,探讨扩张型心肌病患者的冠状动脉循环特点及血流储备(CFR)功能。方法 正常对照组15例,扩张型心肌病组12例。应用TEE测定冠状动脉前降支血流频谱,以基础状态下(R)和潘生丁负荷后(D)冠状动脉舒张期最大流速比值(D/R PDV)为CFR的指标。结果 与对照组比较,扩张型心肌病D/R PDV明显减低(3.43±0.62 vs 2.15±O.75,P<0.01)。扩张型心肌病组D/R PDV与心率负相关(r=-O.73,P相似文献   

临界性高血压患者冠状动脉血流储备功能的研究

目的 :了解无症状临界性高血压患者是否有冠状动脉功能异常。方法 :经食管超声心动描记术研究 2 0例正常人 (正常对照组 )及 17例无症状临界性高血压患者 (临界性高血压组 )的冠状动脉血流储备 (CFR)。以潘生丁静脉注射后和静息时舒张期的最大血流速度比率 (D/R PDV)和收缩期最大血流速度比率 (D/R PSV )作为CFR指标。结果 :1两组受检者静息时的 PDV无显著性差异〔(43± 10 ) m m/s∶ (46± 8) mm /s,P >0 .0 5〕;2静脉注射潘生丁后临界性高血压组的 D/R PDV、D/R PSV较正常对照组明显减少 ,两组之间有显著性差异 (D/RPDV:2 .2 5± 0 .36∶ 2 .86± 0 .42 ,D/R PSV:2 .0 0± 0 .2 6∶ 2 .5 6± 0 .41,P<0 .0 5 )。结论 :无症状临界性高血压患者 CFR能力降低。     

经胸超声心动图对川崎病患儿冠状动脉血流动力学的评估分析

目的探讨经胸超声心动图(TTDE)对川崎病患儿冠状动脉血流动力学的评估价值。方法选择我院接诊的33例川崎病患儿为观察组(左冠状动脉无病变13例,病变恢复10例,持续病变10例),选择同期在我院就诊的32例非川崎病患儿为对照组,比较两组患儿静息状态下冠状动脉左前降支(LAD)、舒张期平均流速(MDV)和峰值流速(PDV)、LAD舒张期血流储备,并分析三磷酸腺苷(ATP)负荷前、后血流速度储备(CFVR)值。结果持续病变组MDV、PDV均明显高于病变恢复组、无病变组和对照组,差异具有统计学意义(P 0. 05); ATP负荷后心率、心率血压乘积较负荷前均明显提高,差异具有统计学意义(P 0. 05);持续病变组CFVR(MDV)和CFVR(PDV)均低于病变恢复组和无病变组、对照组,差异具有统计学意义(P 0. 05)。结论川崎病患儿存在冠状动脉血流储备降低,行TTDE检查能检测不同病变程度患儿的冠状动脉血流动力学变化情况,可为临床治疗提供参考依据。     

高血压病心肌微血管功能损害的研究

目的探讨高血压病患者是否存在心肌微血管病变以及其与疾病严重程度和心肌肥厚的关系.方法应用心肌对比超声心动图,静注含氟碳气体声振白蛋白微泡造影剂(全氟显)后,采用间断谐波成像技术测量静息时和注射潘生丁后心肌的A、β和A*β值,并计算出A、β比值和冠脉微血管的血流储备(CMVFR).结果高血压病患者静息时的A、β和A*β值均较对照组增高(P>0.05),而注射潘生丁后明显降低(P<0.01),A、β比值以及CMVFR显著降低(P<0.05和0.01);随着高血压病情的加重,A和A*β值增高,A比值和CMVFR下降,A和A*β值与SBP、DBP显著正相关(P<0.01)、CMVFR与DBP负相关(\%P\%<0.05);高血压左室肥厚(LVH)患者静息状态的A、β和A*β值较无肥厚者增加,A、β比值和CMVFR下降;A和A*β与LVM和LVMI显著相关(P<0.01);CMVFR与室间隔厚度负相关(P<0.05).结论高血压病患者静息时的心肌微循环血流量增加、心肌微血管储备功能和非内皮依赖性的血管扩张能力明显受损、心肌毛细血管密度明显减少,并且随着疾病的进展而加重;高血压LVH患者较无LVH者的微血管功能受损程度更严重.     

经食管超声多普勒测定冠状动脉储备功能对冠状动脉病变程…

经食管超声（ＴＥＥ）＋潘生丁药物试验测定冠状动脉的血流速度，并根据冠状动脉最大扩张时的血流速度／基础状态下的血流速度之比值来计算冠状动脉储备功能（ＣＦＲ）的指数。我们先后对４４例胸痛待查的患者进行了冠状动脉造影和ＴＥＥ＋潘生丁药物试验，３８例（８６％）的病人获得了满意的ＴＥＥ图像。根据冠状动脉造影的结果将３５例患者分为二组：Ａ组１７例为左前降支狭窄≥５０％或（和）左回旋支狭窄者；Ｂ组２１例为左室状     

冠状动脉造影正常而心电图有心肌缺血改变的临床研究

目的 以计帧法定量评价心电图有心肌缺血改变而冠状动脉造影(CAG)正常者的临床意义.方法 20例静息心电图或平板运动试验(TET)有缺血改变(连续2个及以上相关导联ST段水平型或下斜型下移≥0.05mV或T波深倒置)但CAG正常者为缺血组(A组).50例有心绞痛样症状而心电图、TET及CAG正常者为对照组(B组):测定缺血相关性冠脉血流计帧值(TIMI-FC).并用双密的前降支、下壁缺血者的右冠状动脉及高侧壁缺血者的左冠状动脉回旋支血流的TIMI-FC值显著＞对照组,分别为(34.2±15.6)、(18.7±12.5),P＜0.05;(38.1±11.03)、(21.3±13.8),P＜0.05;及(35.2±15.8)、(18.2±12.6),P＜0.01;TIMI-FC测定结果以＜27为血流正常(NCF);≥27为血流缓慢(SCF).结果 SCF者21例,21例中潘生丁治疗2w后症状缓解及ST-T改善者14例(70%);SCF中心电图有缺血者15例(71.4%).显著多于NGF中心电图有缺血者5例(11.1%);NCF中心电图正常者44例(88.9%),显著多于SCF中心电图正常者6例(28.6%),P＜0.01.结论 CAG正常而心电图有缺血改变者的相关冠脉血流缓慢,提示血流缓慢可作为心肌缺血的指标之一,潘生丁可改善这类患者的症状.     

高血压左室肥厚患者冠状动脉血流储备研究

用电子计算机分析造影剂前缘移动平均速度和冠脉内径测定冠脉血流,发现高血压伴左室肥厚组（14例）静息时左前降支血流量和右冠脉血流速度、血流量高于血压正常对照组（26例）。注射罂粟碱后,高血压组两支血管的血流速度和血流量与对照组相似,但血流储备明显减低。因此,高血压左室肥厚患者的冠脉血流储备减低,可能与这些患者静息时冠脉血流增高有关。     

实时心肌声学造影检测高血压心肌微血管功能

目的:通过实时心肌声学造影(MCE),检测有心绞痛症状而冠状动脉造影(CAG)正常的高血压患者心肌微血管功能. 方法:入选有心绞痛症状而CAG正常的患者12例(高血压组),心绞痛症状不典型而CAG正常的非高血压患者8例(对照组),采用声学造影剂声诺维进行实时MCE检查,分别测定静息状态和腺苷负荷后造影剂微泡达到峰值的平台期强度(A),再充盈平均速度(β)及A·β,并测定A比值、β比值和冠状动脉血流储备(CFR)值.结果:高血压组静息时反映局部心肌血容量的A值、反映局部心肌血流量的A·β值与对照组差异无统计学意义(P>0.05),而反应局部心肌血流速度的β值小于对照组(P<0.05),反应心肌血容量储备的A比值、反应心肌血流速度储备的β比值较对照组低(P<0.05),高血压组CFR低于对照组(P<0.01).结论:有心绞痛症状而CAG正常的高血压患者心肌缺血与心肌微血管密度下降、CFR减退有关,实时MCE可定量检测心肌微血管功能.     

应用TL-201心肌显像定量分析方法检测冠心病患者左室暂时性扩大

目的探讨TL-201心肌显像播生丁试验定量分析方法在检测左室暂时性扩大中的应用价值。方法应用SPECT对82例老年冠心病患L其中心肌梗塞组63例；无心肌梗塞组19例)及10例健康老年人进行TL-201心肌显像，采用定量方法计算左室腔面积(CAV)、左室外周总面积(EPI)及其比值(C／E值)。结果正常对照组静息显像C／E值0.21±0.05；潘生丁试验C／E值为0.22±0.05。82例冠心组中有7例出现一过性C／E值异常，占8．5％a结论冠心病TL-201心叽显像潘生丁试验定量分析方法有可能成为检测左室暂时性扩大评估预后的可靠方法。     

胸痛患者冠状动脉血流储备的超声研究

目的 :应用多平面经食管多普勒超声心动图 (TEE)潘生丁负荷试验 ,探讨胸痛患者的冠状动脉 (冠脉 )循环特点及血流储备 (CFR)功能。方法 :将受试者分为 4组 :冠脉前降支重度狭窄 (A组 ) 10例 ,轻度狭窄 (B组 ) 6例 ,X综合征 (C组 ) 7例 ,冠脉造影正常 (对照组 ) 15例。应用TEE测定冠脉前降支血流频谱 ,以基础状态下(R)和潘生丁负荷后 (D)冠脉舒张期最大流速比值 (D/RPDV)为CFR的指标。结果 :与对照组比较 ,其他 3组基础状态时冠脉血流速度差异无显著性意义 ;CFR明显减低 ,以A组最为明显〔(1.5 5± 4 3)∶(3.4 3± 0 .6 2 )cm/s,P<0 .0 0 1〕 ,狭窄程度与D/RPDV高度相关 (r =0 .83,P <0 .0 0 1) ;B组与C组比较 ,CFR减低程度一致〔(2 .6 2± 0 .71)∶(2 .19± 0 .36 )cm/s,P >0 .0 5 )〕。结论 :CFR反映了冠脉狭窄时冠脉的血流动力学改变 ,可用于判断冠脉狭窄的程度 ;CFR减低是冠脉造影正常患者胸痛的原因     

肺静脉血流定量评定左室舒张功能的临床研究

目的:探讨肺静血流频谱评价高血压病患者左室舒张功能减退程度的价值。方法:确诊的原发性高血压病患者69例根据超声心动图检查结果被分为左室肥厚组(LVH)和无肥厚组,28例健康志愿者作为正常对照组。应用HPSonos2500型超声诊断仪和2.5MHz超声探头记录心尖四腔切面,二尖瓣口和右上肺静脉入口处多普勒血流图。结果:(1)不同组间二尖瓣血流频谱各指标无差别。高血压LVH组较无LVH组及正常组肺静脉血流AR波持续时间(ARD)显著延长(110.21±18.39∶89.78±20.12、90.93±13.11,P<0.01),ARD/AD(A波持续时间)显著增大(1.18±0.40∶0.91±0.19、0.81±0.20,P<0.01);S波流速积分(VTIs)/S、D波流速积分之和(VTIs+VTId)较其它两组低(0.51±0.09∶0.62±0.12、0.60±0.11,P<0.01);(2)在二尖瓣血流正常的高血压病患者中,左室肥厚组较之无肥厚组二尖瓣血流E/A比值显著增大(1.37±0.37∶1.06±0.65;P<0.01);肺静脉血流频谱的ARD、ARD/AD(ARD:120.15±26.60∶82.37±16.38,P<0.05;ARD/AD:1.38±0.34∶0.73∶0.25,P<0.01)明显增大。结论:综合二尖瓣及肺静脉血流频谱可以更全面反应左室的舒张功能,检测不同程度的舒张功能不全。     

Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease

Invasive Doppler catheter-derived coronary flow reserve, echocardiographic measurements of left ventricular hypertrophy and intravenous dipyridamole-limited stress thallium-201 scintigraphy were compared in 48 patients (40 were hypertensive or diabetic) with clinical ischemic heart disease and no or minor coronary artery disease. Abnormal vasodilator reserve (ratio less than 3:1) occurred in 50% of the study group and markedly abnormal reserve (less than or equal to 2:1) occurred in 27%. Coronary vasodilator reserve was significantly lower (2.2 +/- 0.8 versus 3.5 +/- 1.3, p = 0.003) and indexed left ventricular mass significantly higher (152.6 +/- 42.2 versus 113.6 +/- 24.0 g, p = 0.0007) in patients with a positive (n = 11) versus a negative (n = 32) thallium perfusion scan. Coronary flow reserve was linearly related in coronary basal flow velocity as follows: y = -0.17x + 4.59; r = -0.57; p = 0.00002. The decrement in flow reserve was not linearly related to the degree of left ventricular hypertrophy. Abnormal vasodilator reserve subsets found in hypertensive patients were defined on the basis of basal flow velocity, indexed left ventricular mass and clinical factors. In this series, diabetes did not cause a detectable additional decrement in flow reserve above that found with hypertension alone. These findings demonstrate that thallium perfusion defects are associated with depressed coronary vasodilator reserve in hypertensive patients without obstructive coronary artery disease. Left ventricular hypertrophy by indexed mass criteria is predictive of which hypertensive patients are likely to have thallium defects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular remodeling impairs coronary flow reserve in hypertensive patients

BACKGROUND : In arterial hypertension, changes in both left ventricular mass and geometry may occur. Concentric left ventricular remodeling (i.e. an increased wall thickness relative to end diastolic diameter) has been implicated as an independent cardiovascular risk factor in hypertensive patients. The influence of concentric remodeling on the coronary microcirculation is not known. OBJECTIVE : To investigate the impact of left ventricular geometry on coronary flow reserve in patients with arterial hypertension and angiographically normal coronary arteries. METHODS : Following exclusion of coronary artery disease by cardiac catheterization, coronary flow reserve (dipyridamole, 0.5 mg/kg body weight intravenously; argon gas-chromatographic method) was measured in 49 patients with arterial hypertension and in six age-matched controls. Hypertensive patients were grouped by echocardiographic findings according to left ventricular mass and relative left ventricular wall thickness (i.e. left ventricular posterior wall plus septal thickness divided by end diastolic diameter): seven patients had normal left ventricular mass and geometry, 19 had eccentric hypertrophy (i.e. normal relative wall thickness but increased mass), concentric remodeling (i.e. normal mass but increased relative wall thickness) was present in nine patients, and 14 patients had concentric hypertrophy. RESULTS : There was a marked reduction in coronary flow reserve in all hypertensive groups as compared with control values (4.2 +/- 0.5). Within the hypertensive subgroups, the coronary flow reserve was differentially reduced in the following rank order: concentric remodeling (2.0 +/- 0.7) approximately concentric hypertrophy (2.3 +/- 0.8) < eccentric hypertrophy (2.9 +/- 0.6) mu normal geometry (2.7 +/- 0.4). Multi-factorial regression analysis showed that the relative wall thickness but not left ventricular mass was independently linked to the coronary flow reserve. CONCLUSIONS : Concentric left ventricular remodeling is an independent predictor of the coronary flow reserve in hypertensive patients with chest pain and normal coronary angiogram. The impairment of the coronary microcirculation may contribute to the excess cardiovascular event rate associated with hypertensive concentric left ventricular remodeling.     

冠状动脉造影正常的老年高血压患者负荷试验的分析

目的　探讨老年高血压患者冠状动脉储备功能 (CFR)。方法　冠状动脉造影正常的高血压患者 76例 ,无左心室肥厚 (LVH) 32例 (Ⅰ组 ) ,合并LVH44例 (Ⅱ组 ) ,正常对照组 2 6例 (Ⅲ组 )。三组受检者分别行静态、运动心肌核素断层显像及心电图潘生丁负荷试验。结果　心肌核素显像 :Ⅰ组运动后单光子发射型计算机断层仪 (ECT)呈缺血性改变 3例 (9.4% ) ,Ⅱ组运动后ECT呈缺血性改变 11例 (2 5 .0 % ) ,有反向再充填现象 2例 (4.5 % ,P <0 .0 5 )。心电图潘生丁试验 :Ⅰ组阳性 1例 (3.1% ) ,可疑阳性 3例 (9.4% ) ;Ⅱ组阳性 7例 (15 .9% ) ,可疑阳性 9例(2 0 .5 % ,P<0 .0 5 )。心电图潘生丁试验阳性或可疑阳性伴ECT缺血性改变 :Ⅰ组 :无 ;Ⅱ组 8例 (18.2 % ,P <0 .0 1)。正常对照组心肌核素显像及潘生丁试验均无异常。结论　高血压患者存在不同程度CFR下降 ,合并LVH尤为明显 ,其原因可能与冠状动脉微循环结构及功能异常有关。     

Early impairment of coronary flow reserve and increase in minimum coronary resistance in borderline hypertensive patients

OBJECTIVE: To evaluate relations between coronary flow velocity and myocardial oxygen demand at rest, as well as coronary vasodilator capacity and flow reserve, in asymptomatic subjects with borderline hypertension as compared to normotensive controls and patients with sustained high blood pressure (HBP) and without left ventricular hypertrophy (LVH). SUBJECTS AND METHODS: Forty-two asymptomatic males were studied: 13 healthy normotensive volunteers; 12 subjects with borderline HBP and 17 asymptomatic subjects with sustained systemic hypertension. Coronary flow velocity in left anterior descending artery and coronary flow reserve were assessed by transesophageal echo-doppler at baseline and during intravenous adenosine infusion. Left ventricular mass, peak systolic wall stress (PSWS; Pa), and midwall fractional shortening (MFS; %) were obtained from M-mode images of the left ventricle in transthoracic long-axis view and in transesophageal transgastric view. RESULTS: Coronary flow velocity at baseline was not significantly different in the three groups, despite significantly higher rate-pressure product (RPP) in the hypertensive groups as compared with controls. Only in control subjects, was resting coronary flow velocity significantly correlated with RPP (y = 4279 + 200x, r = + 0.58, P < 0.05) and PSWS (y = 17.2 + 5.1 x, r = + 0.62, P < 0.05). Coronary reserve was 3.5 +/- 0.65 in controls and significantly lower (P < 0.05) in borderline hypertensive (2.87 +/- 0.46) and in sustained hypertensive subjects (2.66 +/- 0.56). Minimum coronary resistance was significantly increased in both hypertensive groups (1.30 +/- 0.29 and 1.39 +/- 0.48 mmHg/s per cm) as compared to normotensive controls (0.93 +/- 0.20 mmHg/s per cm, P < 0.01). CONCLUSIONS: In asymptomatic subjects with borderline hypertension and without LVH, a significant reduction in coronary flow reserve is already detectable and appears almost entirely related to an impaired coronary vasodilator capacity rather than to an increased myocardial oxygen demand.     

Decreased mid-to-late diastolic decay of diastolic coronary artery flow velocity in pressure-overloaded left ventricular hypertrophy

Summary This study was carried out to investigate the characteristics of coronary arterial flow in left ventricular hypertrophy secondary to systemic hypertension. The blood velocities in the left anterior descending coronary artery (LAD) were measured by a No. 3F 20 MHz Doppler catheter in 23 hypertensive patients with left ventricular hypertrophy (systolic/diastolic pressure: 181 ± 15/100 ± 4 mmHg) and 13 patients with atypical chest pain, but without left ventricular hypertrophy and any abnormal hemodynamic findings. All patients had normal coronary arteriograms. The LAD blood velocity waveforms in pressure overloaded left ventricular hypertrophy were characterized by both a decreased mid-to-late diastolic deceleration rate (V/T) and a normalized value of V/T by peak diastolic velocity [V/(T · Vpeak)], as well as delayed early diastolic inflow (time for diastolic rise; TDR). The values of the V/(T · Vpeak) in the patients with hypertensive left ventricular hypertrophy and in the normotensive controls were 1.26 ± 0.61 and 3.03 ± 1.18/s, respectively (P < 0.001). The TDR was 145 ± 56 and 66 ± 15 ms (P < 0.001). In patients with hypertensive left ventricular hypertrophy, the V/(T · Vpeak) correlated well with the degree of hypertrophy (r = 0.75,P < 0.01) and with the TDR (r = 0.82,P < 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity increased with the V/(T · Vpeak) (r = 0.68,P < 0.01). In conclusion, the increase in blood flow in the later part of diastole may compensate for the decrease in early diastolic inflow and may cause the reduction in the coronary flow reserve in pressure-overloaded LV hypertrophy.Supported, in part, by Kawasaki Medical School Grant (No. 1-102) for Project Research, Japan.     

Evaluation of coronary flow reserve in hypertensive patients by dipyridamole transesophageal doppler echocardiography

This study evaluates the coronary flow reserve (CFR) in hypertensive patients with and without left ventricular (LV) hypertrophy. CFR was assessed by transesophageal Doppler echocardiography in 15 normal subjects (group I), 21 hypertensive patients without LV hypertrophy (group II), and 27 hypertensive patients with LV hypertrophy (group III). All hypertensive patients were complaining of typical anginal pain and had normal coronary angiograms. The sample volume was placed at the bifurcation of the left main and left anterior descending coronary arteries. Coronary blood flow velocities were evaluated at rest, 2 minutes after dipyridamole infusion, and 2 minutes after intravenous aminophylline. The ratios of dipyridamole to rest peak diastolic and systolic velocities were considered as indexes of CFR. Peak diastolic velocity ratio was significantly lower in group III than in groups I and II (1.6 +/- 0.2, 2.7 +/- 0.4, and 2.1 +/- 0.2, respectively; p <0.05), and it was significantly lower in group II than I (p <0.05). The peak systolic velocity ratio was significantly lower in group III than in groups I and II (1.7 +/- 0.3, 2.8 +/- 0.3, and 2.1 +/- 0.2, respectively; p <0.05), and it was significantly lower in group II than I (p <0.05). The peak diastolic velocity ratio was inversely related to systolic blood pressure, diastolic blood pressure, and LV mass index (r = -0.48, -0. 51, and -0.37 respectively) in hypertensive patients. It is concluded that CFR is significantly impaired in hypertensive patients, especially those with LV hypertrophy, compared with healthy subjects. The degree of impairment of CFR is related to LV mass index.     

Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics.

STUDY OBJECTIVE--The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN--Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS--23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS--The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS--(1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.     

Left ventricular hypertrophy secondary to systemic hypertension: its effect on coronary hemodynamics]

To clarify the characteristics and possible causes of phasic blood velocity patterns in pressure overload hypertrophy, we measured blood flow velocities in the left anterior descending coronary arteries in 16 patients with left ventricular hypertrophy secondary to systemic hypertension. These measurements were made with a 20MHz Doppler catheter. All patients had normal coronary arteriograms. The blood flow velocity patterns were characterized by the decrease in the rise of early diastolic inflow velocity. Prolongation in the time from the onset of diastole to peak velocity (TDPV) correlated with the degree of left ventricular hypertrophy. TDPV was prolonged in proportion to the increase in the peak left ventricular systolic pressure and left ventricular ejection fraction. The flow reserve calculated from the ratio of the diastolic mean velocity after the intracoronary injection of papaverine to the resting flow showed a trend toward the decrease proportional to the prolongation in TDPV due to an increase of wall thickness. In conclusion, preceding systolic vascular compression and systolic vascular strain can be factors causing early diastolic inflow disturbance in left ventricular hypertrophy secondary to hypertension. The decrease of coronary reserve may partially be attributable to the decrease in the rise of early diastolic inflow velocity.