直立倾斜试验阳性的排尿性晕厥患者血流动力学及自主神经的反应

目的:通过观察排尿性晕厥(MS)患者在直立倾斜试验中发生晕厥时心率、血压以及心率变异性(HRV)的变化,探讨MS的发病机制并对临床治疗提出新的思路。方法:对16例MS患者及20例健康者行基础直立倾斜试验和硝酸甘油诱发直立倾斜试验。试验全程行无创血压、心电监测,每3min行HRV分析。结果:16例MS患者中6例出现阳性反应,晕厥前心率达到最高,平均为(105.67±19.68)次/min,晕厥时心率比最高心率下降了(50.32±12.5)%,而SBP、DBP、MAP分别下降了(17.62±4.65)%、(16.87±6.31)%、(17.27±4.96)%。健康对照组无一例发生阳性反应。HRV分析发现,倾斜70°后,阳性反应组低频段功率标化值(LFn)和低频与高频功率标化值(HFn)的比值(LFn/HFn)均增大,HFn减小;晕厥前或结束前LFn和LFn/HFn值升至最高,HFn降至最低;晕厥时LFn与LFn/HFn急剧下降,而HFn迅速升高。健康对照组试验过程中仅有LFn与LFn/HFn的轻微变化,且与倾斜试验开始前基础状态相比差异无统计学意义。结论:MS的发生与自主神经调节功能障碍(迷走神经过度兴奋、交感神经张力不足)密切相关。在积极预防MS发作的基础上加用抗胆碱药物和自主神经调节药物,可望取得一定疗效。     

硝酸甘油激发的倾斜试验在血管迷走性晕厥中的应用

目的:了解在倾斜试验中,用硝酸甘油进行激发对于血管迷走性晕厥(VVS)患者的诊断价值,并通过观察VVS患者晕厥前后的血流动力学改变及心率变异性功率谱变化,以探讨VVS的发病机制。方法:55例不明原因反复发作晕厥患者(病例组)及20例健康者(对照组)行直立倾斜试验,倾斜75°持续45min,阴性者舌下含服0.3mg硝酸甘油后倾斜至75°持续20min,观察有无阳性反应。倾斜过程中动态监测心电图、血压和心率,并进行心率变异性分析。结果:病例组55例中32例出现阳性反应(阳性率为58.2%),8例于基础倾斜试验阶段出现阳性反应,24例于硝酸甘油激发后出现阳性反应;32例中,血管抑制型(VD型)21例,心脏抑制型(CI)5例,混合型(MX)6例。对照组20例中4例出现阳性反应。病例组中CI型患者倾斜后心率上升,达高峰后在短期内急剧下降,发生晕厥,血压也略下降;MX型患者晕厥时心率及血压均在短期内急剧下降;VD型患者晕厥时血压在短期内急剧下降,心率也发生一定程度的下降,下降百分比小于CI型及MX型(P<0.05)。倾斜后阳性者低频标化植(LFnorm)增高,高频标化值(HFnorm)下降,低高频比值(LF/HF)增高,晕厥前LFnorm及LF/HF达到最大值,HFnorm达到最低值,晕厥时LFnorm及LF/HF显著下降,HFnorm增加。结论:硝酸甘油激发能增加倾斜试验的阳性率,自主神经功能改变(交感活性迅速减退,迷走神经兴奋)为晕厥产生的主要机制,并在不同患者产生不同的血流动力学改变。     

硝酸甘油激发的倾斜试验在血管迷走性晕厥中的应用

目的了解在倾斜试验中,用硝酸甘油进行激发对于血管迷走性晕厥(vasovagalsyncope,VVS)患者的诊断价值,通过观察VVS患者晕厥前后的血流动力学改变及心率变异性功率谱变化,探讨VVS的发病机制。方法55例不明原因,反复发作的晕厥患者及20例健康人行直立倾斜试验,倾斜75°持续45min,阴性者舌下含服0.3mg硝酸甘油后倾斜至75°持续20min,观察有无阳性反应。倾斜过程中动态监测心电图、血压和心率,并进行心率变异性分析。结果病例组55例中32例出现阳性反应,8例于基础倾斜试验阶段出现阳性反应,24例于硝酸甘油激发后出现阳性反应,阳性率从14.55%升高到58.18%。阳性反应中,血管抑制型(VD)21例,占65.63%,心脏抑制型(CI)5例,占15.63%,混合型(MX)6例,占18.75%。对照组20例中4例出现阳性反应。CI型患者倾斜后心率上升,达高峰后在短期内急剧下降,发生晕厥,血压也略下降;MX型患者晕厥时心率及血压均在短期内急剧下降;VD型患者晕厥时血压在短期内急剧下降,心率也发生一定程度的下降,下降百分比小于CI型及MX型(P<0.05)。倾斜后阳性组LFnorm增高,HFnorm下降,LF/HF增高,晕厥前LFnorm及LF/HF达到最大值,HFnorm达到最低值,晕厥时LFnorm及LF/HF显著下降,HFnorm增加。结论硝酸甘油激发能增加倾斜试验的阳性率,自主神经功能改变(交感活性迅速减退,迷走神经兴奋)为晕厥产生的主要机制,并在不同患者产生不同的血流动力学改变。     

改良硝酸甘油直立倾斜试验对70岁及以上人群血管迷走性晕厥的诊断价值

目的探讨改良硝酸甘油直立倾斜试验(MNHUT)对70岁及以上人群血管迷走性晕厥(VVS)的诊断价值。方法184例70岁及以上不明原因晕厥患者随机分成常规硝酸甘油直立倾斜试验(CNHUT)组(99例)和MNHUT组(85例)。CNHUT包括基础倾斜(BHUT)45 min,平卧位舌下喷雾硝酸甘油400μg,再行硝酸甘油倾斜(NHUT)20 min;MNHUT包括BHUT 10 min,倾斜位舌下喷雾硝酸甘油400μg,继续NHUT 20 min。结果两组BHUT、NHUT及倾斜试验总阳性率差异无统计学意义(P0.05)。CNHUT组BHUT、NHUT及倾斜试验总无结果的发生率均多于MNHUT组(P0.05),MNHUT组依从率优于CNHUT组(P0.05)。MNHUT组倾斜及试验总时程较CNHUT组明显缩短。结论 MNHUT敏感性与CNHUT相同,倾斜及试验总时程大幅缩短,显著提高了老年患者直立倾斜试验的效率及依次性,适用于70岁及以上VVS患者的诊断。     

45例血管迷走性晕厥病人倾斜试验临床分析

目的对血管迷走神经(VS)病人的直立倾斜试验(HUT)进行临床分析.方法将45例不明原因晕厥的病人和40例健康人对照,进行基础倾斜试验(BHUT)和硝酸甘油舌下含服激发倾斜试验,观察血压、心率.结果BHUT组阳性率为13.3%,HUT加硝酸甘油含服组阳性率为51.1%,总阳性率64.4%,对照组阳性率为2.5%,晕厥组与对照组比较有统计学意义(P＜0.01).结论HUT对血管迷走神经性晕厥的诊断有较好的价值.     

基础直立倾斜试验与舌下含服硝酸甘油直立倾斜试验诊断血管迷走性晕厥的价值

目的:探讨基础直立倾斜试验(HUT)与舌下含服硝酸甘油直立倾斜试验(SNHUT)对血管迷走性晕厥(VVS)的诊断价值。方法:对我院2011年至2012年共61例不明原因晕厥,并高度怀疑VVS的患者(晕厥组)进行直立倾斜试验,。并以22例健康者作为健康对照组。结果:晕厥组61例患者中倾斜试验阳性57例,阳性率达到93.44%。其中HUT阳性16例(26.23%),SNHUT阳性41例(67.21%)。22例健康对照组也同样进行这两试验,其中HUT阳性1例(4.54%),SNHUT阳性3例(13.63%)。晕厥组SNHUT阳性率高于HUT的,但无显著差异(χ2=0.175,P=0.683)。结论:直立倾斜试验是目前诊断血管迷走性晕厥的一种无创,重复性强,容易被患者所接受的较好方法。配合舌下含服硝酸甘油直立倾斜试验可提高试验的阳性率。     

血压与心率基础值对直立倾斜试验阳性结果的影响

目的探讨血压与心率基础值对直立倾斜试验阳性结果的影响。方法不明原因晕厥病人51例,行45min基础直立倾斜试验(head-uptilttest,HUT),阴性病人保持70°倾斜角,直接含服硝酸甘油0.25mg,继续20min试验;HUT阳性病人按晕厥反应类型分为血管抑制型组、心脏抑制型组与混合型组。比较基础血压和基础心率。按血压140/90mmHg与心率(60次/分)为界分别分为高血压组与非高血压组,心率偏慢组与心率正常组。结果HUT阳性组率为62.7%(32/51),其中血管抑制型21例;心脏抑制型5例;混合型6例;阴性19例。HUT阳性组病人的血压与心率基础值与HUT阴性者差异无统计学意义(P>0.05)。晕厥发生率:高血压组62%(8/13),血压正常组63%(24/38),差异无统计学意义;心率偏慢组3/5,心率正常组60%(29/46),差异无统计学意义。结论血压与心率基础值对HUT没有明显影响,不能作为HUT试验阳性的预测指标。     

舌下含服硝酸甘油直立倾斜试验对血管迷走性晕厥的诊断价值

为寻找使用方便、省时、耐受性良好的倾斜方案 ,将不明原因晕厥者 91例、无晕厥史者 5 2例 (对照 )分别随机分为异丙肾上腺素组 (A组 ,患者 45例、对照 2 6例 )和硝酸甘油组 (B组 ,患者 46例、对照 2 6例 )。每组首先行 70°30min的基础倾斜试验 (BHUT) ,若为阴性则加用药物激发。A组在BHUT结束后将倾斜床放回水平位 ,静脉注射异丙肾上腺素 (剂量 3μg/min) 5min ,再次倾斜 70° 10min。B组在BHUT结束后同一倾斜角度给予硝酸甘油 0 .2mg舌下含服 ,持续倾斜 2 0min。结果 :A组BHUT阳性率为 11.1% (5 / 45 ) ,加用药物后阳性率为 42 .2 % (19/ 45 ) ;总敏感性5 3 .3 %、特异性 88.5 % ;3例 (6 .7% )出现胸闷、胸痛不能耐受试验。B组BHUT阳性率为 10 .9% (5 / 46 ) ,加用药物后阳性率为 45 .7% (2 1/ 46 ) ;总敏感性 5 6 .5 %、特异性 92 .3%。结论 :含服硝酸甘油激发试验具有良好的敏感性和特异性 ,且使用方便、省时、耐受性好 ,可做为诊断血管迷走性晕厥的常规方法。     

直立倾斜试验诊断晕厥的探讨

目的研究直立倾斜试验(HUTT)对血管迷走性晕厥(VVS)的诊断价值。方法入选2016年12月至2018年12月在本院就诊,不明原因晕厥,疑似VVS的患者124例,进行HUTT,包括基础倾斜试验(BHUT)和舌下含服硝酸甘油直立倾斜试验(SNHUT)。结果 124例受试者中,阴性反应57例,阳性反应66例,1例为体位性心动过速。阳性组的女性比例较高(p0.05);阳性组最快心率高于阴性组(p0.05),阳性组结束时的心率、收缩压、舒张压均低于最大值(p0.05),也明显低于阴性组(p0.05)。阳性反应中,BHUT就出现阳性反应的5例,占8%;SNHUT阳性61例,占92%;按反应类型:血管抑制性28例(42%),心脏抑制性9例(14%),混合型29例(44%)。3例受试者出现长RR间歇,最长达10.7s,2例受试者舌下含服硝酸甘油后出现腹痛不适。结论 HUTT对VVS具有较好的诊断价值,SNHUT能显著提高VVS的检出率。     

114例女性血管迷走性晕厥患者的临床特征及转归情况分析

目的分析114例女性血管迷走性晕厥(VVS)患者的临床特征及转归情况。方法选取江苏大学附属武进医院心内科2002年5月—2014年6月收治的114例女性VVS患者,直立倾斜试验(HUTT)检查资料完整。入院后均进行相关治疗,出院前均进行系统宣教,随访至2014年9月。回顾性分析其年龄分布情况、HUTT检查结果、疾病分型、晕厥前诱因、晕厥先兆症状、HUTT检查时晕厥及晕厥先兆症状、随访时转归情况。结果年龄分布:12~19岁8例、20~29岁4例、30~39岁10例、40~49岁31例、50~59岁21例、60~69岁28例、≥70岁12例。HUTT检查结果:基础倾斜试验阶段阳性30例,药物激发试验阶段阳性84例。疾病分型:血管抑制型(VD型)53例(46.5%),心脏抑制型(CI型)12例(10.5%),混合型(MX型)49例(43.0%)。50例(43.9%)患者就诊前晕厥发作1次。89例(78.1%)患者晕厥前有具体诱因,其中部分患者有多种诱因。98例(86.0%)患者有晕厥先兆症状,其中胸闷、头晕和全身出汗为最常见的3个先兆症状。110例(96.5%)患者在行HUTT检查时出现晕厥或晕厥先兆症状,其中64例(58.2%)患者同时出现3种或3种以上的先兆症状。78例患者获得随访,其中70例患者未再次发生晕厥,8例患者仍有晕厥发生。结论了解女性VVS患者的发病特点有助于临床尽早明确诊断,且系统的宣教能有效预防VVS跌倒伤害事件的发生。     

Dynamic changes in the QT interval during the head-up tilt test in patients with vasovagal syncope

Dynamic changes of the QT and QTc interval as well as QT dispersion and QTc dispersion during the head-up tilt test were investigated in 15 patients (8 men, mean age 32 years) with vasovagal syncope (VVS) and a positive head-up tilt test and in a control group of 15 patients with syncope in the case-history and a negative head-up tilt test (9 men, mean age 33 years). The value at rest of the QT interval did not differ in patients with VVS and controls. In controls at the beginning of HUT shortening of QT occurred (0.447 sec. vs. 0.419 sec. p = 0.0002), subsequently the QT did not change significantly. In patients with VVS during the beginning of the test only an insignificant shortening of QT occurred, while during the development of the syncope QT was prolonged (0.394 sec. vs. 0.420 sec. p < 0.0001). QT corrected for the pulse rate (QTc) did not change significantly during HUT. QTc dispersion was in patients with VVS significantly lower 3 minutes before the development of the syncope (0.067 sec. vs. 0.085 sec. p = 0.03), which may indicate the decline of the sympathetic and increase of the parasympathetic tonus which subsequently leads to the development of vasovagal syncope. QTc dispersion before the test was higher in patients with VVS as compared with controls (0.087 sec. vs. 0.063 sec., p = 0.03), which suggests an increase in the baseline sympathetic tonus in patients with VVS.     

Plasma galanin response to head-up tilt in normal subjects and patients with recurrent vasovagal syncope

Neurohumoral factors may contribute to cardiovascular changes associated with vasovagal syncope (VVS). Galanin (GAL) is a neuropeptide, widely distributed in the central and peripheral nervous systems, that interacts with both sympathetic and vagal systems as well as with neurotransmitters, such as serotonin. We investigated the changes in plasma GAL and catecholamine levels during head-up tilt (HUT) test in patients with recurrent VVS. Twenty-two patients (11 women, aged 33.1 +/- 4.2 years) with a history of VVS and 10 healthy subjects (5 women, aged 38.0 +/- 5.8 years) underwent HUT test (60 degrees, 45 minutes). GAL and catecholamine plasma levels were measured in the supine position, during HUT and, in patients with positive response, at presyncope, syncope, and after recovery of consciousness. Thirteen patients developed syncope during HUT, whereas no healthy subjects had a positive response. In healthy subjects, GAL did not change during HUT. By contrast, in patients with a history of VVS and a negative response to tilting (no syncope), GAL significantly (P <.001) increased in response to tilting (supine, 10.2 +/- 0.6 pmol/L; tilting, 18.1 +/- 1.1 pmol/L at 45 minutes) and correlated positively with the increases in blood pressure (BP) and heart rate (HR). In patients with a positive response, GAL did not change either before the loss of consciousness or during syncope. In patients with a positive response, norepinephrine (NE) significantly (P <.001) increased during tilting and then remained practically unchanged during syncope, whereas epinephrine (E) significantly (P <.001) increased during tilting and then showed further significant increases at presyncope and syncope. In conclusion, this study shows that circulating GAL levels progressively increase in correlation with the cardiovascular parameters during a negative HUT in patients with a history of VVS, whereas they remain unchanged in healthy subjects. Moreover, in the patients with tilting-induced syncope GAL does not change either before or during loss of consciousness. These data suggest a role for endogenous GAL in the adaptive responses to acute orthostatic stress preventing syncope in susceptible individuals.     

Role of the serotonergic system in the genesis of vasovagal syncope.

AIMS: The hypotensive reflex responsible for vasovagal syncope appears related to a reduction in sympathetic neural outflow. Several animal studies suggest that serotonin may play a role in the genesis of this reflex, through inhibition of sympathetic activity. However, the role of the serotonergic system is unknown in humans. The purpose of the study was to investigate the role of the serotonergic system in the genesis of vasovagal syncope by means of the level of platelet and plasma serotonin, as well as plasma catecholamines, during tilt-induced syncope. METHODS AND RESULTS: Fifteen patients (age 34 +/- 16 years) with vasovagal syncope underwent a head-up tilt test (HUT, 60 degrees , 45 min). If syncope did not develop, 300 microg nitroglycerin was administered sublingually and patients continued to be tilted for a further 20 min. Blood samples were obtained in the supine position, and then after 3, 10, 15, 30, 45, 48 and 65 min of HUT. If syncope developed, blood samples were obtained at the beginning of the prodrome, during syncope and after the recovery of consciousness. Platelet and plasma serotonin and plasma catecholamines were measured using high-pressure liquid chromatography with electrochemical detection. Ten patients developed syncope during the unmedicated HUT and four after nitroglycerin. In these patients plasma adrenaline significantly increased from the last programmed sample before the prodrome to its beginning and showed a further increase during loss of consciousness, whereas plasma noradrenaline did not increase, as an expression of inhibition of sympathetic neural outflow. In the patients experiencing syncope, both platelet and plasma serotonin showed no significant change after tilt-up, at the beginning of prodrome, during syncope and after recovery of consciousness. CONCLUSION: These results do not suggest that the serotonergic system plays a role in the pathophysiology of vasovagal syncope.     

Syncope induced by tobacco smoking in the head-up position.

A 26-year-old man had a loss consciousness for a few minutes while smoking in the standing position, and was referred to hospital. No abnormalities were found in a computed tomography examination of his head, in a 24-h electrocardiogram or in an exercise tolerance test. The head-up tilt test (HUT) while tobacco smoking elicited a positive response in the tilted position, but the HUT without tobacco smoking was negative. The most noteworthy effect of tobacco smoking during the HUT was the high level of plasma epinephrine compared to the levels seen during supine smoking or the HUT alone. Syncope induced by tobacco smoking in the standing position is rare and the mechanism may be the same as that underlying neurally mediated syncope.     

An implantable loop recorder study of highly symptomatic vasovagal patients: the heart rhythm observed during a spontaneous syncope is identical to the recurrent syncope but not correlated with the head-up tilt test or adenosine triphosphate test.

OBJECTIVES: The aim of this study was to analyze the heart rhythm during spontaneous vasovagal syncope (VVS) in highly symptomatic patients with implantable loop recorders (ILR) and to correlate this rhythm with the heart rhythm observed during head-up tilt test (HUT). BACKGROUND: Heart rhythm obtained during provocative condition is often used to guide therapy in VVS. To date there is no conclusive evidence that the heart rhythm observed during a positive HUT can predict heart rhythm during VVS or that the heart rhythm observed during a spontaneous syncope will be identical to the recurrent syncope. METHODS: Twenty-five consecutive VVS patients (age 60.2 +/- 17.1 years; 14 women,) presenting with frequent syncopes (6.9 +/- 4.6 episodes/year) and a positive HUT (cardioinhibitory in 8 patients) were implanted with an ILR. Seven of them also had a positive adenosine triphosphate (ATP) test. RESULTS: Follow-up was 17.0 +/- 3.6 months. Thirty VVS were observed in 12 patients. Nine episodes showed bradycardia of <40 beats/min or asystole; progressive sinus bradycardia preceding sinus arrest was the most frequent electrocardiographic finding. Twenty-one syncopes occurred without severe bradycardia. The heart rhythm observed during the first syncope was identical to the recurrence. No correlation was found between slow heart rate at the ILR interrogation and a cardioinhibitory HUT response (p = 1.0) or a positive ATP test (p = 1.0). CONCLUSIONS: In highly symptomatic patients with VVS, the heart rhythm observed during spontaneous syncope does not correlate with the HUT. The heart rhythm during the first spontaneous syncope is identical to the recurrent syncope.     

Different mechanisms of isoproterenol-induced and nitroglycerin-induced syncope during head-up tilt in patients with unexplained syncope: important role of epinephrine in nitroglycerin-induced syncope

INTRODUCTION: A reduction in left ventricular volume and an increase in epinephrine levels have been reported in tilt-induced neurally mediated syncope. To compare the mechanisms of isoproterenol-induced and nitroglycerin-induced syncope during head-up tilt and to investigate the role of catecholamines, the temporal changes in plasma levels of norepinephrine and epinephrine and in left ventricular volume were measured. METHODS AND RESULTS: The first study population consisted of 90 patients with syncope of unknown etiology and 12 control subjects. The second study population consisted of 43 patients with unexplained syncope. In the first study, head-up tilt (80 degree angle) was conducted for 40 minutes, and norepinephrine and epinephrine levels were measured. In the second study, all patients were randomly allocated to either isoproterenol test (20 patients) or nitroglycerin test (23 patients) for 20-minute head-up tilt. Isoproterenol infusion was given at a rate of 1 to 3 microg/min. Intravenous infusion of nitroglycerin was started at 250 microg/hour with increasing dosages up to 1,500 microg/hour. Norepinephrine and epinephrine were measured in peripheral venous blood. Left ventricular volumes were measured by echocardiography with patients in the supine position and during head-up tilt every 1 minute. End-diastolic volume and end-systolic volume were calculated. In the first study, 61 patients demonstrated a positive response and 29 patients demonstrated a negative response. Plasma norepinephrine changes during head-up tilt were not significantly different, whereas epinephrine levels were significantly higher in the positive patients than in the negative and control subjects (148 +/- 118 pg/mL vs 66 +/- 31 pg/mL and 55 +/- 27 pg/mL). Thirteen of the 20 patients given isoproterenol and 15 of the 23 patients given nitroglycerin showed a positive head-up tilt (65.0% vs 65.2%; P = NS). During isoproterenol and nitroglycerin infusion head-up tilt, epinephrine in the positive group determined by the nitroglycerin test was significantly higher than that in the other three groups (103 +/- 38 pg/mL vs 60 +/- 33 pg/mL, 31 +/- 21 pg/mL, and 50 +/- 52 pg/mL). In contrast, end-systolic volume was significantly smaller in the positive group than in the other three groups based on findings of the isoproterenol test. CONCLUSION: The findings suggest that nitroglycerin triggers head-up tilt-induced syncope by increasing epinephrine levels, whereas isoproterenol induces syncope by decreasing left ventricular volume.     

Tilt testing in neurocardiogenic syncope: isosorbide versus isoproterenol

OBJECTIVE: To compare the diagnostic value of pharmacological stimulation with sublingual isosorbide dinitrate and intravenous isoproterenol during tilt testing in patients with neurocardiogenic syncope and with a negative tilt test without pharmacological provocation. METHODS AND RESULTS: One hundred and twenty patients with a history of neurocardiogenic syncope (aged 15 to 77 years) and 50 healthy volunteers (aged 25 to 70 years) were prospectively submitted to head-up tilt (HUT). Those who did not develop syncope or presyncope during passive HUT for 30 minutes underwent repeated HUT with isoproterenol infusion at 4 microg/min (ISOP HUT), for 10 minutes, and, subsequently, were tilted after sublingual administration of 5 mg of isosorbide dinitrate (ISDN HUT) for another 12 minutes. ISDN HUT was always performed after ISOP HUT. Sensitivity and specificity of passive HUT were 41% (95% C.I. 32.9% to 51.0%) and 100%, respectively. Sensitivity of ISOP HUT was 51.4% (95% C.I. 39.2% to 63.6%) and specificity 70% (95% C.I. 55.4% to 82.1%) and for ISDN HUT were 70% (95% C.I. 57.9% to 80.4%) and 88% (95% C.I. 75.7% to 95.5%), respectively. The accuracy of ISDN HUT was significantly higher than the accuracy of ISOP HUT 77.5% (95% C.I. 68.9% to 84.6%). There were fewer side effects during ISDN HUT. CONCLUSION: Sublingual isosorbide dinitrate is at least as sensitive as isoproterenol to assess patients with suspected neurocardiogenic syncope and with a negative tilt test without provocation. The low rate of side effects and the higher accuracy of ISDN HUT, along with the simplicity of this challenge compared to ISOP HUT, suggest that sublingual isosorbide dinitrate should be preferred as a provocative agent to evaluate neurocardiogenic syncope after a negative passive tilt test.     

Methodology of head-up tilt testing potentiated with sublingual nitroglycerin in unexplained syncope

Shortened head-up tilt testing (HUT) potentiated with sublingual nitroglycerin (60 degrees passive standing for 20 minutes followed, if negative, by 400 microg of sublingual nitroglycerin spray with the test continuing for another 20 minutes) differs from conventional nitroglycerin HUT for a shorter drug-free phase (20 vs 45 minutes). To compare the positivity rate of the 2 protocols, both tests were performed in a randomized sequence in 10 patients with unexplained syncope (study 1), and another 42 patients were randomly assigned either to conventional or to shortened nitroglycerin HUT (study 2). To evaluate the reproducibility of the shortened nitroglycerin HUT, another 38 patients with unexplained syncope underwent 2 consecutive tests within a 7+/-8 day interval (study 3). Finally, to evaluate the specificity of the test, 47 control subjects underwent shortened nitroglycerin HUT (study 4). Seven positive responses were observed during shortened nitroglycerin HUT, and there were 8 positive responses during conventional nitroglycerin HUT (p = NS) in the study 1 group. Fifteen positive (71%) responses, 5 negative responses, and 1 exaggerated response were observed during shortened nitroglycerin HUT; 16 positive (76%, p = NS vs. shortened nitroglycerin HUT), 3 negative, and 2 exaggerated responses were observed during conventional nitroglycerin HUT in the study 2 group. During the first test, 21 patients (55%) had a positive, 15 patients had a negative, and 2 patients had an exaggerated response in study group 3. During the second test, 15 positive (39%), 19 negative, and 4 exaggerated responses were observed. Thus, the reproducibility was 67% for a positive and 94% for a negative test. In control subjects, 2 positive (4%) responses, 38 negative, and 7 exaggerated responses were observed with a specificity of 96% in study group 4. In patients with unexplained syncope, shortened nitroglycerin HUT allowed a positivity rate similar to that of the conventional test. Moreover, the shortened test provided a high specificity and adequate reproducibility for both the positive and the negative responses.     

Transient modification of baroreceptor response during tilt-induced vasovagal syncope.

AIMS: Normally, arterial baroreceptors attempt to minimize systemic hypotension by initiating reflex vasoconstriction and tachycardia. However, in the setting of vasovagal syncope (VVS), these usual compensatory mechanisms either fail to be triggered or the response is inadequate. We hypothesized that in VVS prone individuals, arterial baroreceptor response (BRR) is normal under most conditions, but that a transient functional BRR disturbance occurs during an evolving vasovagal faint and may in part account for failure of the usual compensatory response. METHODS AND RESULTS: This study assessed BRR in the baseline state and again in association with either VVS induced head-up tilt (HUT) or after a prolonged period of upright posture without VVS. To minimize impact on HUT outcome, BRR was estimated non-pharmacologically by measuring blood pressure and heart rate changes, induced when subjects were returned to the supine position after undergoing diagnostic 70 degrees HUT evaluation. Beat to beat heart rate and arterial blood pressure changes were recorded in 13 patients with syncope and another 16 individuals with negative HUT (control group). Baseline BRR was initially evaluated at the end of a 3 min symptom free HUT (HUT#1), and the measurement was repeated after a 45 min duration HUT in the control group or in conjunction with syncope in VVS prone individuals (HUT#2). Baseline BRR did not differ significantly in controls and VVS prone individuals (controls: 3.37+/-1.56, VVS prone: 6.0+/-2.02 ms/mmHg, p=0.27). Further, at the end of 45 min HUT#2, BRR was unaltered from baseline in control subjects (4.92+/-1.36 ms/mmHg, p=0.48), but was markedly reduced from baseline value in individuals who experienced a faint, -3.30+/-0.81 ms/mmHg (p<0.0003 vs baseline). CONCLUSION: Compared with individuals who do not manifest VVS during HUT, VVS prone individuals appear to demonstrate functional diminution of baroreceptor responsiveness. This altered response may undermine the normal expected compensatory response to evolving systemic hypotension. The basis for this transient disturbance in baroreceptor responsiveness is currently unknown.