Vasodepressor cough syncope masked by sleep apnea-induced asystole

Vasodepressor Cough Syncope. Cough syncope is classified among the neural-reflex "situational" faints, but whether the clinical consequences in affected individuals result from reflex triggered bradyarrhythmia or vasodepressor-induced hypotension, or both, is often unknown. In this report we describe findings in a patient with a clinical history consistent with cough syncope, and in whom documented multiple asystolic spells were at first believed to be responsible for symptoms. However, pacemaker therapy initiated at an outside facility failed to suppress symptoms, and subsequent referral for more detailed autonomic study revealed the asystole to be due to sleep apnea, whereas cough-induced vasodepressor hypotension was the basis of syncope in this individual; the latter provided a pathophysiologic target for prevention of recurring symptoms. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1024-1027, September 2012).     

Mechanisms of cough syncope as evaluated by valsalva maneuver

Successful treatment of cough syncope depends on the correction of various pathogenetic mechanisms among different patients. The valsalva maneuver (VM), which elicits hemodynamic responses mimicking coughs, has potential for investigating the individual pathogenesis of cough syncope. Eighteen consecutive patients suffering from cough-induced syncope were examined. All patients were asked to cough and to perform VM several times under continuous cerebral blood-flow velocity and blood pressure (BP) monitoring by transcranial Doppler and finger plethysmography. Eight patients demonstrated abnormal VM characterized by the absent BP overshoot following the relief of straining. Patients demonstrating abnormal VM had delayed BP recovery after cough (median, 16.4; range, 8.7-25.6 seconds) compared to those demonstrating normal VM (2.6, 1.3-3.8 seconds, p < 0.001). Seven of the 10 patients exhibiting normal BP overshoot during VM had stenotic arterial lesions in the cerebral or coronary circulation, whereas only one of the eight patients demonstrating absent BP overshoot had coronary artery disease (70% vs. 12.5%, p = 0.025). Other clinical profiles, body mass index, frequency of obstructive pulmonary disease and valsalva ratio did not differ between patients featuring normal and absent BP overshoot. In conclusion, the pathogenesis of cough syncope could be different between patients with normal and abnormal VM responses. Patients who had no BP overshoot during VM sustained prolonged hypotension after cough. The VM helps in discriminating among pathogenic mechanisms and guiding investigation and treatment for cough syncope patients.     

Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope

This study assessed the temporal relation of RR interval, AH interval and systemic blood pressure changes during induced symptomatic bradycardia-hypotension episodes in 14 patients with recurrent syncope suspected of being neurally mediated. Upright tilt with isoproterenol reproduced symptoms in 9 of 14 patients (positive response) and was negative in 5 of 14 (negative response). Isoproterenol alone shortened supine RR intervals in all patients. With tilt, however, isoproterenol prolonged RR intervals in those with positive results (supine 519 +/- 124 ms vs tilt 845 +/- 212 ms, p less than 0.005) while further shortening RR intervals among negative responders (supine 436 +/- 90 ms vs tilt 377 +/- 82 ms, p less than 0.05). Similarly, tilt with isoproterenol prolonged AH intervals in patients with positive responses despite RR prolongation, while shortening AH in negative responders. Additionally, with combined tilt and isoproterenol, systemic arterial pressure decreased significantly in patients with positive responses (systolic 99 +/- 13 vs 57 +/- 13 mm Hg, p less than 0.001, diastolic 62 +/- 17 vs 28 +/- 9 mm Hg, p less than 0.001) but not in patients with negative responses. Further, onset of hypotension (42 +/- 14 seconds after tilt) preceded onset of RR interval prolongation (52 +/- 23 seconds after tilt). Syncope (142 +/- 72 seconds after tilt) coincided closely with nadir of systemic pressure (136 +/- 74 seconds) and both tended to precede maximum RR prolongation (152 +/- 87 seconds). Thus, the bradycardia and hypotension associated with neurally mediated syncope exhibit characteristic but distinctly different time courses, with arterial pressure changes developing earlier and coinciding more closely with symptom development.     

Impaired heart rate responses to cough and deep breathing in elderly patients with unexplained syncope

To test the hypothesis that elderly patients with unexplained syncope have impaired autonomic control of heart rate, chronotropic responses to deep breathing and cough were studied in 12 elderly patients (85 +/- 4 years), 14 elderly control subjects (82 +/- 7 years) and 10 young subjects (26 +/- 5 years). There was no difference in resting RR interval between elderly patients with syncope and control subjects. However, the ratio of the maximum RR/minimum RR (an index of heart rate variability) during deep breathing was significantly lower in patients than in control subjects (p less than 0.005). In the minute following cough, there was no difference in initial reflex tachycardia, but subsequent rebound bradycardia was blunted in the elderly patients with syncope. The predominant impairment in elderly patients with unexplained syncope was the bradycardia component of the responses to deep breathing and cough, suggesting that these patients may have impaired parasympathetic modulation of heart rate. Although not likely to be the cause of syncope in these patients, these findings may reflect an underlying autonomic defect.     

The autonomic and hemodynamic effects of oral theophylline in patients with vasodepressor syncope.

Adenosine appears to be an important mediator of hypotension and bradycardia in certain subsets of patients with vasodepressor syncope. Adenosine receptor blockage with methylxanthines may hypothetically prevent the vasodepressor spell. We studied the chronotropic, hemodynamic, and cardiac autonomic responses to head-up tilt in patients (mean age 40.7 +/- 18.1 years) with vasodepressor syncope before and after treatment with oral theophylline. At baseline, hypotension and syncope or near syncope were induced at 11.7 +/- 2.3 minutes of 60 degrees head-up tilt in all patients. Cardiac vagal and sympathetic tone showed biphasic and directionally opposite changes during tilt. Repeat tilt during oral theophylline therapy (6-12 mg/kg/day for 14 +/- 6 days) did not provoke symptomatic hypotension in 82% of patients. During 10.7 +/- 6.1 months of follow-up, seven patients had no recurrence of vasodepressor syncope and seven patients discontinued theophylline because of adverse reactions. Low-dose theophylline prevents tilt-induced vasodepressor syncope and may prevent spontaneous vasodepressor syncope in selected patients who can tolerate theophylline.     

Reproducibility of asystole during head-up tilt testing in patients with neurally mediated syncope.

Tilt induced prolonged asystole has been considered to identify a distinct subgroup of patients with neurally mediated syncope and management including permanent pacemaker implantation has been suggested. To evaluate the reproducibility of asystolic response during head-up tilt testing (HUT), 33 patients with neurally mediated syncope and asystolic response (> or = 3 seconds) during HUT prospectively underwent two consecutive tests 13 +/- 15 days apart. On repeat tilt testing asystole was reproduced in 12 patients (36%), while 8 patients still had a positive HUT, but without asystole. Remarkably, 13 patients (40%) had a negative repeat HUT. Among 12 patients with asystole on both HUTs there was no significant difference in duration of asystole (14 371 +/- 11 430 ms vs 13 707 +/- 10 470 ms, P = ns) and time to syncope (36 +/- 20 min vs 37 +/- 20 min, P = ns) during initial and repeat HUTs. In conclusion, asystole during tilt testing does not seem to be a reproducible response.     

Cough frequency, cough sensitivity and health status in patients with chronic cough

BACKGROUND: Little is known about the frequency of cough in health and in patients with chronic cough. METHODS: We measured cough frequency and its relationship with other markers of cough severity in 20 patients with chronic cough and 9 healthy subjects using the Leicester Cough Monitor (LCM), which is an automated ambulatory digital cough monitor that records sound only. All subjects had a 6-h recording and recordings were manually counted. A subgroup of 6 normals and 6 patients with a stable chronic cough had repeat measurements up to 6 months apart. RESULTS: Mean (sem) cough counts/hour were 43(8) in patients with chronic cough and 2(1) in normals (mean difference 41; 95% confidence interval 24-59; P<0.001). The cough counts were repeatable (within subject standard deviation: 23 coughs/hour; intraclass correlation coefficient 0.8). Cough counts correlated significantly with physical (r=-0.6, P=0.03), social (r=-0.7, P=0.01) and total Leicester Cough Questionnaire (LCQ) health status scores (r=-0.6, P=0.03) and cough sensitivity (concentration of capsaicin causing 5 coughs: r=0.9, P=0.008). CONCLUSION: We have shown that there are marked differences in cough frequency between patients with chronic cough and healthy subjects, that these measurements are repeatable, and that they correlate with cough-specific health status.     

辣椒素咳嗽激发试验方法的建立及其安全性评价

目的探讨辣椒素咳嗽激发试验的方法并评价其安全性。方法采用吸气触发的定量吸入装置,对60名健康志愿者(A组)、11例上呼吸道感染患者(B组)、10例胃-食管反流性咳嗽患者(C组)以及10例支气管哮喘(简称哮喘)患者(D组)行辣椒素咳嗽激发试验。所有受试者逐步吸入雾化浓度倍增(1.95、3.90、7.80、15.6、31.2、62.5、125、250、500、1 000μm ol/L)的辣椒素溶液,测试期间记录咳嗽次数。将诱发产生≥5次咳嗽的最低浓度(C5)作为咳嗽阈值,以对数值lg C5判断咳嗽反射的敏感性。在咳嗽激发前、后进行常规肺通气功能以及多频脉冲振荡呼吸阻力测定。结果全部受试者中仅6例出现轻微不适,其中1例有烧灼感、2例恶心和3例声嘶。咳嗽激发前A、B、C、D组患者第一秒用力呼气容积(FEV1)、呼吸总阻抗(Zrs)分别为(3.6±0.5)L、(2.6±0.8)mm Hg.L-1.s-1、(3.7±0.7)L、(2.5±0.5)mm Hg.L-1.s-1、(2.7±0.8)L、(2.7±0.8)mm Hg.L-1.s-1、(2.1±0.8)L,(3.3±1.5)mm Hg.L-1.s-1,经激发后分别为(3.6±0.5)L、(2.7±0.7)mm Hg.L-1.s-1、(3.7±0.8)L、(2.6±0.3)mm Hg.L-1.s-1、(2.6±0.7)L、(2.7±0.7)mm Hg.L-1.s-1、(2.1±0.8)L、(3.7±2.0)mm Hg.L-1.s-1,各组激发前、后FEV1、Zrs比较差异均无统计学意义(P均>0.05)。A、B、C、D组的咳嗽敏感性lg C5分别为2.45±0.46、2.51±0.20、1.52±0.70、2.34±0.56,其中C组与A、B、D组比较差异有统计学意义(P均<0.01);而A、B、D组间比较差异无统计学意义(P均>0.05)。结论定量吸入辣椒素咳嗽激发试验安全、可行,可在临床上用于咳嗽敏感性的测定。     

Methodology of head-up tilt testing in patients with unexplained syncope

Prolonged 60 degree head-up tilt has been shown to be valuable in the investigation of unexplained syncope, diagnosing neurally mediated bradycardia/hypotension or malignant vasovagal syndrome. To evaluate the methodology of tilt testing, the following were examined: reproducibility of results, tilt duration, angle of tilt, method of tilt support and effect of age in patients and control subjects. Seventy-one patients with recurrent unexplained syncope underwent 60 min of 60 degree tilt; 53 (75%) had an abnormal test with vasovagal syncope at 24 +/- 10 min (mean +/- SD). Tilting to 60 degrees resulted in an abnormal test in only 2 (7%) of 27 control subjects without cardiovascular symptoms (p less than 0.001); and 5 (15%) of 34 patients with syncope and documented conduction tissue disease (p less than 0.001). Of 15 youthful fainters, 3 (20%) had vasovagal reactions as did 1 (8%) of 12 asymptomatic youthful control subjects. These 12 control subjects also underwent tilting with a saddle support and 7 (67%) had vasovagal reactions. It is concluded that the duration of tilting at 60 degrees should be 45 min (mean time to syncope +2 x SD in the 53 patients with abnormal results). Twenty percent of patients with an abnormal tilt test may not demonstrate syncope with repeat tilting. Saddle tilt testing in unexplained syncope may result in a loss of specificity. Tilting at less than 60 degrees results in a loss of sensitivity. Head-up tilt may be less useful in youthful subjects with vasovagal syncope than in other subjects.     

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.     

Hemodynamic significance of heart rate in neurally mediated syncope

BACKGROUND: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. METHODS: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). RESULTS: The baseline hemodynamic data (mean +/- standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 +/- 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 +/- 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 +/- 0.29 vs. 1.97 +/- 0.41 1/min/m2, p < 0.001 and 2098 +/- 615 vs. 1573 +/- 353 dynes x s x cm(-5) x m2, p < 0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. CONCLUSIONS: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope.     

Comparison of hemodynamic adaptation to orthostatic stress in patients with hypertrophic cardiomyopathy with or without syncope and in vasovagal syncope

This study was designed to investigate whether, in patients with hypertrophic cardiomyopathy (HC), tilt-induced volume unloading triggers a peripheral reflex similar to that seen in patients with a history of vasovagal syncope or rather acts through an intrinsic cardiac mechanism secondary to diastolic dysfunction. Thirty-seven patients with HC (10 with and 27 without a history of syncope), 10 patients with vasovagal syncope, and 9 controls underwent 70° head-up tilt for 45 minutes during continuous radionuclide monitoring of left ventricular function. We focused on the initial 5 minutes into the tilt test, well before symptoms occurred, to exclude that the observed hemodynamic changes were the consequence rather than the cause of syncope. HC patients with previous syncope and vasovagal patients experienced significant hypotension after the initial 5 minutes of tilt. Only HC patients with a history of syncope had a significant decrease in cardiac output, which began at the initial stage of the test. Systemic vascular resistance decreased in vasovagal patients, but increased in the HC syncopal group. Baseline peak filling rate was lower (2.4 ± 0.5 vs 3.3 ± 1.1 stroke counts/s, P = 0.03) and a “pseudonormal” or a restrictive pattern of left ventricular filling was more frequent (70% vs 26%, P = 0.02) in HC patients with than without a history of syncope. Thus, significant hypotension or frank syncope during orthostatic stress in HC patients with a history of syncope is due to an early decrease in cardiac output, which occurs well before the onset of symptoms; such impaired hemodynamic adaptation seems to be related to diastolic dysfunction.     

Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope : pacemaker versus no therapy: a multicenter randomized study. The Vasovagal Syncope International Study (VASIS) Investigators

BACKGROUND-This study was performed to compare implantation of a DDI pacemaker with rate hysteresis with no implant in respect to syncopal recurrences in patients with severe cardioinhibitory tilt-positive neurally mediated syncope. METHODS AND RESULTS-Forty-two patients from 18 European centers were randomized to receive a DDI pacemaker programmed to 80 bpm with hysteresis of 45 bpm (19 patients) or no pacemaker (23 patients). Inclusion criteria were >/=3 syncopes over the last 2 years and a positive cardioinhibitory (Vasovagal Syncope International Study types 2A and 2B) response to tilt testing. The median number of previous syncopal episodes was 6; asystolic response to tilt testing was present in 36 patients (86%) (mean asystole, 13.9+/-10.2 seconds). All patients were followed up for a minimum of 1.0 years and a maximum of 6.7 years (mean, 3.7+/-2.2). One patient (5%) in the pacemaker arm experienced recurrence of syncope compared with 14 patients (61%) in the no-pacemaker arm (P=0.0006). In the no-pacemaker arm, the median time to first syncopal recurrence was 5 months, with a rate of 0.44 per year. On repeated tilt testing performed within 15 days after enrollment, positive responses were observed in 59% of patients with pacemakers and in 61% of patients without pacemakers (P=NS). CONCLUSIONS-In a limited, select group of patients with tilt-positive cardioinhibitory syncope, DDI pacing with hysteresis reduced the likelihood of syncope. The benefit of the therapy was maintained over the long term. Even in untreated patients, the syncopal recurrence burden was low. A negative result of tilt testing was not a useful means to evaluate therapy efficacy.     

Cardiovascular and catecholamine responses to head-up tilt in the diagnosis of recurrent unexplained syncope in elderly patients

To increase understanding of the mechanisms causing syncope in patients over the age of 60, hemodynamic and hormonal responses to 60 minutes of 60 degree head-up tilt were examined in 10 patients with recurrent syncope of unknown origin and five controls with no history of syncope. Nine of 10 patients and all five controls experienced orthostatic intolerance on the tilt table. Syncope or pre-syncope occurred later in controls than in those syncope patients who had exact reproduction of their clinical symptoms (median time 52 versus 22 minutes, P = 0.05). Three different mechanisms of orthostatic intolerance were identified in the 14 subjects: (1) vasovagal syncope, n = 9 (sudden hypotension +/- bradycardia); (2) dysautonomic syncope, n = 3 (immediate and gradual parallel declines in both systolic and diastolic pressures with blunted increase in heart rate); (3) psychogenic or vestibular reaction, n = 2 (orthostatic intolerance without hemodynamic changes). Vasovagal syncope patients showed a significant increase in plasma norepinephrine from baseline to maximum level during tilt (100 +/- 39% increase, P = 0.03) and a subsequent decrease at the time of syncope (30 +/- 5% decrease, P = 0.01), while plasma epinephrine increased markedly from baseline to the time of syncope (827 +/- 154% increase, P = 0.0003). Dysautonomic syncope patients had lower supine levels of norepinephrine compared to vasovagal syncope patients (182 +/- 30 versus 614 +/- 146 pg/mL, P = 0.008) and no significant change in norepinephrine over time; epinephrine levels increased significantly less than in vasovagal patients (net change 38 +/- 8 versus 189 +/- 56 pg/mL, P = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)     

Investigation of a hemodynamic basis for syncope in hypertrophic cardiomyopathy. Use of a head-up tilt test.

BACKGROUND. Syncope and sudden death in hypertrophic cardiomyopathy may have a hemodynamic basis. The presence of a small ventricular cavity with high intracavity pressures may activate left ventricular baroreceptors and cause reflex hypotension as described in other populations with syncope. METHODS AND RESULTS. To investigate this potential mechanism of syncope in hypertrophic cardiomyopathy, we studied 17 patients with a history of syncope (syncopal), 19 without syncope (nonsyncopal), and nine normal control subjects by using a head-up tilt test. Head-up tilt at 60 degrees for 45 minutes was followed by 10-minute tilts during incremental doses of isoprenaline. Heart rate, blood pressure, and two-dimensional and Doppler echocardiography were monitored throughout. On tilting, hypertrophic cardiomyopathy patients showed a decline in mean arterial pressure of -5 +/- 6 mm Hg (p less than 0.001) compared with no change in control subjects (0.2 +/- 6 mm Hg, p = 0.9). Left ventricular outflow tract velocity decreased on tilting in control subjects (-8 +/- 6 cm/sec, p = 0.004) but increased in the syncopal and nonsyncopal patients (20 +/- 50 cm/sec, p = 0.05). Reflex hypotension with or without bradycardia, associated with syncope or presyncope, was induced in seven syncopal patients, two nonsyncopal patients, and two control subjects (p = 0.05). The early response to tilt in these subjects was characterized by maintenance of blood pressure but a greater increase in left ventricular fractional shortening than in the other subjects (10 +/- 8% versus 1 +/- 1%, p = 0.002). The onset of hypotension was associated with a trend toward further decreases in left ventricular diameters, outflow tract velocity, and transmitral flow velocities. In the remaining patients who had a negative test, transient hypotension (systolic pressure less than 100 mm Hg) occurred in seven syncopal patients and three nonsyncopal patients compared with none of the control subjects (p = 0.01). In total, hypotension was demonstrated in 82% of syncopal patients compared with 26% of nonsyncopal patients and 22% of control subjects (p = 0.001). CONCLUSIONS. Patients with hypertrophic cardiomyopathy and a history of syncope frequently display hypotension during head-up tilt. In some cases, sudden hypotension occurs and is usually associated with bradycardia and a reduced cavity size, findings compatible with activation of a ventricular baroreflex. In other cases, transient hypotension occurs and could be explained by an impairment of baroreceptor function. These mechanisms may contribute to the occurrence of syncope in daily life.     

Daily oral care and cough reflex sensitivity in elderly nursing home patients

BACKGROUND: Intensive oral care can reduce the incidence of pneumonia in elderly nursing home patients, but the mechanism is unknown. OBJECTIVE: To explore the effects of intensive oral care on impaired cough reflex sensitivity, which is a known risk factor of aspiration pneumonia. METHODS: Cough reflex sensitivity to citric acid was measured in elderly nursing home patients, who were randomly assigned to the intervention group (n = 30) and the control group (n = 29). The patients in the intervention group had their teeth and gingiva cleaned by caregivers after every meal for 1 month. The patients in the control group performed their own oral care during the same period. Serum substance P (SP) concentration, cognitive function, and activities of daily living (ADL) were also assessed. RESULTS: In the intervention group, cough reflex sensitivity at 30 days showed significantly higher sensitivity than baseline (p < 0.01). At 30 days, the cough reflex sensitivities in the intervention group were significantly higher than that of the control group (p < 0.05). Compared with the control group, the odds ratio of improvement of cough reflex sensitivity was 5.3 (95% confidence interval, 1.7 to 16.0; p < 0.005) for the intervention group. One month of intensive oral care did not have a significant effect on serum SP concentration, cognitive function, and ADL. CONCLUSION: Intensive oral care may reduce the incidence of pneumonia by improving cough reflex sensitivity in elderly nursing home patients.     

Enalapril-induced cough is associated with non-severe heart failure

The incidence of enalapril-induced cough was evaluated in 199 patients with congestive heart failure. Cough was more frequent in class I or II patients (28%) than in class III (4.1%, p<0.01) and class IV (0%, p<0.01) patients. Brain natriuretic peptide level was lower in patients in the cough (+) group than in the cough (-) group (170+/-107 vs. 538+/-637 pg/ml, p<0.01). The incidence of enalapril-induced cough is low in patients with severe congestive heart failure and a cough can be a marker of non-severe heart failure.     

激素敏感性咳嗽和非激素敏感性咳嗽的临床特征分析

目的 探讨激素敏感性咳嗽（CSRC）和非激素敏感性咳嗽（NCSRC）的临床特征差异.方法 收集2003年至2013年在广州医科大学第一附属医院呼吸科就诊的病因明确的357例慢性咳嗽患者的临床资料,进行回顾性分析.依据病因分为激素敏感性咳嗽组和非激素敏感性咳嗽组,将两组的临床特征进行比较.结果 与非激素敏感性患者相比,激素敏感性咳嗽患者的咳嗽病程更短（24 vs.36个月,P=0.025）,CSRC组日间咳嗽积分更低（P＜0.05）.NCSRC组的咳嗽常于白天出现（87.85％ vs.78.15％,P=0.006）,而CSRC组的咳嗽则常出现于夜间（43.13％ vs.32.60％,P=0.018）.与NCSRC组相比,CSRC组胃食管反流症状的发生率更低（26.33％ vs.54.14％,P=0.000）,咳嗽与饮食相关的比例更低（11.43％ vs.37.08％,P=0.000）,伴有鼻部症状的比例更低（40.06％ vs.55.8％,P=0.001）,气促的比例更高（18.21％ vs.11.05％,P=0.032）.感冒和讲话引起咳嗽或咳嗽加重的比例均为NCSRC组高于CSRC组（48.62％ vs.38.94％,28.73％ vs.17.65％,P均＜0.05）.CSRC组咽部异物感、频繁清喉和咽喉壁黏液附着感的比例显著低于NCSRC组（分别为8.68％ vs.18.23％,20.73％ vs.40.88％,3.64％ vs.10.50％,P均＜0.01）.CSRC组的MMEF/pred显著低于NCSRC组（72.29±31.22vs.84.09±31.64,p=0.000）,且气道高反应性的比例高于NCSRC组（29.9％ vs.4.26％）.CSRC组中痰嗜酸粒细胞百分比明显高于NCSRC组（中位数5％ vs.0.25％,P=0.001）.结论 激素敏感性咳嗽和非激素敏感性咳嗽的临床特征存在一定差异,但单纯从临床特征上无法完全区分二者,仍需结合相关实验室检查来明确诊断.     

Usefulness of physical maneuvers for prevention of vasovagal syncope.

BACKGROUND: It is known that approximately two-thirds of patients with vasovagal syncope have prodromal symptoms and when these start, physical maneuvers that can increase venous return may abort the syncopal attack. The aims of this study were to evaluate the effects of 3 physical maneuvers, squatting, leg-crossing with muscle tensing, and handgrip, on improving hemodynamic status, and to compare the effect of each on aborting or preventing vasovagal syncope. METHODS AND RESULTS: Of 50 patients who underwent the head-up tilt test (HUT) to evaluate syncope, 27 patients with positive HUT were classified as group I (14 men, 13 women; mean age 44.5+/-15.3 years), 23 patients with negative HUT were classified as group II (13 men, 10 women; mean age 41.2 +/-16.7 years), and 21 normal subjects were classified as group III (10 men, 11 women; mean age 28.6+/-6.3 years). The effects of the physical maneuvers were evaluated in 21 patients from group I who underwent a repeat HUT 1 week after the initial test. Leg-crossing significantly increased systolic blood pressure (SBP) in all 3 groups (8.0+/-5.8 mmHg in group I, 7.0+/-8.5 mmHg in group II, 8.7+/-5.7 mmHg in group III; p < 0.05), but not diastolic blood pressure (DBP). Squatting significantly increased SBP and DBP in all 3 groups (7.1 +/-5.1, 4.6+/-5.8 mmHg in group I, 7.8+/-5.9, 4.3+/-4.7 mmHg in group II, 6.5+/-5.0, 3.7+/-3.9 mmHg in group III; p < 0.05). However, handgrip did not exert any significant influence on the hemodynamics in any group nor did heart rate change significantly during the physical maneuvers in any group. During the repeat HUT, prodromal symptoms with hypotension developed in 13 of the 21 patients and of these 5 fainted immediately after and were not able to do the physical maneuvers. Squatting and leg-crossing aborted syncope in 7 of 8 patients, but handgrip aborted syncope in only 1 patient. CONCLUSION: Squatting and leg-crossing with muscle tensing improved the hemodynamics of normal subjects as well as those of patients with vasovagal syncope. Squatting and leg-crossing can be used as a simple and effective preventive maneuver in patients with vasovagal syncope.     

Impaired efficacy of cough in patients with Parkinson disease

STUDY OBJECTIVES: Aspiration pneumonia, a leading cause of death in patients with Parkinson disease (PD), usually occurs at the advanced stages of the disease. We investigated both motor and sensory components of cough and induced-sputum substance P (SP) concentrations in patients with early and advanced stages of PD to assess whether cough efficacy is impaired in PD. SUBJECTS: Fifteen female patients with early stages of PD (Hoehn and Yahr stage II-III), 10 patients with advanced stages of PD (Hoehn and Yahr stage IV), and 15 age-matched female control subjects were investigated. MEASUREMENTS: The motor component of cough efficacy was assessed by monitoring voluntary maximal cough peak flow. The sensory component of cough efficacy was assessed by measuring cough reflex sensitivity to citric acid inhalation. Sputum SP concentrations were measured in sputum induced by hypertonic saline solution inhalation. RESULTS: The mean (+/- SD) cough peak flow rates in patients with both early PD (230 +/- 74 L/min; p < 0.005) and advanced PD (186 +/- 60 L/min; p < 0.0001) were significantly weaker than that in control subjects (316 +/- 70 L/min). Cough reflex sensitivity in patients with advanced PD (46.7 +/- 49.3 g/L) was significantly lower compared to control subjects (14.5 +/- 16.6 g/L; p < 0.01) and patients with early PD (11.2 +/- 14.8 g/L; p < 0.005). The sputum SP concentration was significantly lower in patients with advanced PD (11.2 +/- 8.4 pg/mL) compared to that in control subjects (35.6 +/- 15.4 pg/mL) and patients with early PD (28.5 +/- 16.4 pg/mL). CONCLUSION: In the early stages of the disease, mainly the motor component of cough was impaired. In advanced stages of the disease, both the motor and sensory components of cough were impaired. Sputum SP concentration significantly declined in patients with advanced PD. The results suggest that the combination of impaired motor and sensory components of cough may play an important role in the development of aspiration pneumonia in PD.