Carotid Sinus Syndrome (carotid + sinus_syndrome)

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Medical Sciences100%

Selected Abstracts

Treatment of Vasodepressor Carotid Sinus Syndrome with Midodrine: A Randomized, Controlled Pilot Study

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2005
Allan Moore MRCPI
Objectives: To evaluate the efficacy of treatment of the vasodepressor form of carotid sinus hypersensitivity (carotid sinus syndrome (CSS)) with midodrine. Design: A prospective, double-blind, randomized, controlled trial of crossover design. Setting: A dedicated outpatient facility with access to tilt-table, digital arterial photoplethysmography, and 24-hour ambulatory blood pressure (BP) monitoring equipment. Participants: Ten older adults (4 male, 6 female, mean age 75, range 66,86 years) with a history of unexplained syncope who displayed an asymptomatic decrease in systolic BP (SBP) of more than 50 mmHg or a symptomatic decrease of more than 30 mmHg within 30 seconds of carotid sinus massage (CSM). Measurements: Symptom reproduction and BP and heart rate changes were evaluated after CSM in supine and semierect positions on the right and then left sides. These measurements were performed on the final day of placebo and active-treatment phases. Ambulatory 24-hour BP monitoring took place on the penultimate and final days of each treatment phase. Results: Eight patients were symptomatic after their initial CSM. The mean±standard deviation SBP decrease after initial CSM was 54±22 mmHg. Initial mean 24-hour ambulatory BP was 127/70±7/5 mmHg. Eight patients reported symptoms after CSM at the end of the placebo phase. The mean SBP decrease at the end of the placebo phase was 49±12 mmHg. The mean 24-hour ambulatory BP was 127/69±9/7 mmHg. One patient reported symptoms after CSM at the end of the active-treatment phase. The mean SBP decrease at the end of the active-treatment phase was 36±9 mmHg. The mean 24-hour ambulatory BP at the end of the treatment phase was 133/75±7/6 mmHg. The differences in symptom reporting and mean SBP decrease after CSM were both significant (P<.01 and P=.03, respectively). Conclusion: The results of this pilot study suggest that treatment of vasodepressor CSS with midodrine significantly reduced the rate of symptom reporting and attenuated SBP decreases after CSM but increased mean 24-hour ambulatory BP. [source]

Paradoxical Vasodilation During Lower Body Negative Pressure in Patients with Vasodepressor Carotid Sinus Syndrome

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 6 2003
Arduino A. Mangoni MD
OBJECTIVES: To elucidate the pathophysiological mechanism of the vasodepressor form (VD) of carotid sinus syndrome (CSS) by maneuvers designed to induce generalized sympathetic activation after baroreceptor unloading (lower body negative pressure, LBNP) or direct peripheral adrenoreceptor stimulation via local administration of norepinephrine (NA). DESIGN: Subjects were identified with VD of CSS through diagnostic testing. SETTING: Research laboratory. PARTICIPANTS: Eleven young controls (YC) (mean age ± standard error of mean = 22.8 ± 0.7), eight elderly controls (EC) (72.6 ± 0.6), and eight elderly patients with VD (78.7 ± 1.7). MEASUREMENTS: Forearm arterial blood flow (FABF) was measured in the left and right arms by venous occlusion plethysmography. Measurements were performed during baseline conditions, LBNP (,20 mmHg), and intra-arterial NA infusion in the left brachial artery at three progressively increasing rates (60, 120, and 240 pmol/min). RESULTS: During LBNP, FABF significantly decreased in YC (baseline 3.61 ± 0.30 vs ,20 mmHg 2.96 ± 0.24 mL/100 g/min, P = .030) and EC (4.05 ± 0.74 vs 3.69 ± 0.65 mL/100 g/min, P = .033) but increased in elderly patients with VD (3.65 ± 0.60 vs 4.54 ± 0.80 mL/100 g/min, P = .020). During NA infusion, a significant forearm vasoconstriction occurred in YC (FABF left:right ratio 1.00 ± 0.05 at baseline; 0.81 ± 0.08 at 60 pmol/min, P = .034; 0.81 ± 0.05 at 120 pmol/min, P < .001; 0.72 ± 0.04 at 240 pmol/min, P < .001), whereas no significant FABF changes were observed in EC (1.04 ± 0.06; 0.96 ± 0.07, P = .655; 0.89 ± 0.10, P = .401; 0.94 ± 0.10, P = .590) or elderly patients with VD (1.04 ± 0.06; 1.16 ±0 .10, P = .117; 1.04 ± 0.08, P = .602; 1.11 ± 0.10, P = .305). CONCLUSION: VD of CSS is associated with a paradoxical vasodilatation during LBNP and an impairment of peripheral ,-adrenergic responsiveness, which may be age-related. [source]

Contribution of a Pacemaker Bradycardia Detection Algorithm in the Study of Patients with Carotid Sinus Syndrome

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001
PIERRE GRAUX
GRAUX, P., et al.: Contribution of a Pacemaker Bradycardia Detection Algorithm in the Study of Patients with Carotid Sinus Syndrome. While carotid sinus syndrome (CSS) is often suspected as a cause of syncope in the elderly, whether it represents an indication for cardiac pacing may remain uncertain. Bradycardia algorithms included in pacemakers are now able to establish a precise relationship between spontaneous asystole and occurrence of symptoms and strengthen the indication for permanent pacing. This study included seven men and three women (70.5 ± 7.3 years of age) who, over an average period of 54.1 ± 17 months, had suffered from syncope (12.6 episodes/patient) and presyncope (11.2 episodes/patient) attributed to pure cardioinhibition (2 patients) or mixed CSS (8 patients). Other sources of symptoms were excluded by thorough clinical evaluations, including Holter monitoring, echocardiography, and electrophysiological testing. All patients received a CHORUS 6234 pacemaker, the memory of which includes a dedicated bradycardia detection algorithm capable of storing atrial and ventricular chains, and date and time of the last ten pauses and/or bradycardic events. After a initial period of 14.7 ± 8 months, during which symptoms were suppressed, the bradycardia algorithm was activated. From then on, a cumulative increase in the number of patients presenting with diurnal pauses was measured (1 month, n = 0; 3 months, n = 6; 9 months, n = 7; 2 years, n = 8). Fourteen episodes of diurnal asystole were recorded. The mean duration of the longest episodes of spontaneous ventricular standstill was 6,319 ± 1,615 ms and was due to sinoatrial block (n = 7), atrioventricular block (n = 5), and a combination of both (n = 2). In conclusion, activation of the CHORUS bradycardia algorithm allowed confirmation of the appropriateness of permanent pacing in a majority of patients suffering from CSS. [source]

Treatment of Vasodepressor Carotid Sinus Syndrome with Midodrine: A Randomized, Controlled Pilot Study

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2005
Allan Moore MRCPI
Objectives: To evaluate the efficacy of treatment of the vasodepressor form of carotid sinus hypersensitivity (carotid sinus syndrome (CSS)) with midodrine. Design: A prospective, double-blind, randomized, controlled trial of crossover design. Setting: A dedicated outpatient facility with access to tilt-table, digital arterial photoplethysmography, and 24-hour ambulatory blood pressure (BP) monitoring equipment. Participants: Ten older adults (4 male, 6 female, mean age 75, range 66,86 years) with a history of unexplained syncope who displayed an asymptomatic decrease in systolic BP (SBP) of more than 50 mmHg or a symptomatic decrease of more than 30 mmHg within 30 seconds of carotid sinus massage (CSM). Measurements: Symptom reproduction and BP and heart rate changes were evaluated after CSM in supine and semierect positions on the right and then left sides. These measurements were performed on the final day of placebo and active-treatment phases. Ambulatory 24-hour BP monitoring took place on the penultimate and final days of each treatment phase. Results: Eight patients were symptomatic after their initial CSM. The mean±standard deviation SBP decrease after initial CSM was 54±22 mmHg. Initial mean 24-hour ambulatory BP was 127/70±7/5 mmHg. Eight patients reported symptoms after CSM at the end of the placebo phase. The mean SBP decrease at the end of the placebo phase was 49±12 mmHg. The mean 24-hour ambulatory BP was 127/69±9/7 mmHg. One patient reported symptoms after CSM at the end of the active-treatment phase. The mean SBP decrease at the end of the active-treatment phase was 36±9 mmHg. The mean 24-hour ambulatory BP at the end of the treatment phase was 133/75±7/6 mmHg. The differences in symptom reporting and mean SBP decrease after CSM were both significant (P<.01 and P=.03, respectively). Conclusion: The results of this pilot study suggest that treatment of vasodepressor CSS with midodrine significantly reduced the rate of symptom reporting and attenuated SBP decreases after CSM but increased mean 24-hour ambulatory BP. [source]

Paradoxical Vasodilation During Lower Body Negative Pressure in Patients with Vasodepressor Carotid Sinus Syndrome

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 6 2003
Arduino A. Mangoni MD
OBJECTIVES: To elucidate the pathophysiological mechanism of the vasodepressor form (VD) of carotid sinus syndrome (CSS) by maneuvers designed to induce generalized sympathetic activation after baroreceptor unloading (lower body negative pressure, LBNP) or direct peripheral adrenoreceptor stimulation via local administration of norepinephrine (NA). DESIGN: Subjects were identified with VD of CSS through diagnostic testing. SETTING: Research laboratory. PARTICIPANTS: Eleven young controls (YC) (mean age ± standard error of mean = 22.8 ± 0.7), eight elderly controls (EC) (72.6 ± 0.6), and eight elderly patients with VD (78.7 ± 1.7). MEASUREMENTS: Forearm arterial blood flow (FABF) was measured in the left and right arms by venous occlusion plethysmography. Measurements were performed during baseline conditions, LBNP (,20 mmHg), and intra-arterial NA infusion in the left brachial artery at three progressively increasing rates (60, 120, and 240 pmol/min). RESULTS: During LBNP, FABF significantly decreased in YC (baseline 3.61 ± 0.30 vs ,20 mmHg 2.96 ± 0.24 mL/100 g/min, P = .030) and EC (4.05 ± 0.74 vs 3.69 ± 0.65 mL/100 g/min, P = .033) but increased in elderly patients with VD (3.65 ± 0.60 vs 4.54 ± 0.80 mL/100 g/min, P = .020). During NA infusion, a significant forearm vasoconstriction occurred in YC (FABF left:right ratio 1.00 ± 0.05 at baseline; 0.81 ± 0.08 at 60 pmol/min, P = .034; 0.81 ± 0.05 at 120 pmol/min, P < .001; 0.72 ± 0.04 at 240 pmol/min, P < .001), whereas no significant FABF changes were observed in EC (1.04 ± 0.06; 0.96 ± 0.07, P = .655; 0.89 ± 0.10, P = .401; 0.94 ± 0.10, P = .590) or elderly patients with VD (1.04 ± 0.06; 1.16 ±0 .10, P = .117; 1.04 ± 0.08, P = .602; 1.11 ± 0.10, P = .305). CONCLUSION: VD of CSS is associated with a paradoxical vasodilatation during LBNP and an impairment of peripheral ,-adrenergic responsiveness, which may be age-related. [source]

Contribution of a Pacemaker Bradycardia Detection Algorithm in the Study of Patients with Carotid Sinus Syndrome

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001
PIERRE GRAUX
GRAUX, P., et al.: Contribution of a Pacemaker Bradycardia Detection Algorithm in the Study of Patients with Carotid Sinus Syndrome. While carotid sinus syndrome (CSS) is often suspected as a cause of syncope in the elderly, whether it represents an indication for cardiac pacing may remain uncertain. Bradycardia algorithms included in pacemakers are now able to establish a precise relationship between spontaneous asystole and occurrence of symptoms and strengthen the indication for permanent pacing. This study included seven men and three women (70.5 ± 7.3 years of age) who, over an average period of 54.1 ± 17 months, had suffered from syncope (12.6 episodes/patient) and presyncope (11.2 episodes/patient) attributed to pure cardioinhibition (2 patients) or mixed CSS (8 patients). Other sources of symptoms were excluded by thorough clinical evaluations, including Holter monitoring, echocardiography, and electrophysiological testing. All patients received a CHORUS 6234 pacemaker, the memory of which includes a dedicated bradycardia detection algorithm capable of storing atrial and ventricular chains, and date and time of the last ten pauses and/or bradycardic events. After a initial period of 14.7 ± 8 months, during which symptoms were suppressed, the bradycardia algorithm was activated. From then on, a cumulative increase in the number of patients presenting with diurnal pauses was measured (1 month, n = 0; 3 months, n = 6; 9 months, n = 7; 2 years, n = 8). Fourteen episodes of diurnal asystole were recorded. The mean duration of the longest episodes of spontaneous ventricular standstill was 6,319 ± 1,615 ms and was due to sinoatrial block (n = 7), atrioventricular block (n = 5), and a combination of both (n = 2). In conclusion, activation of the CHORUS bradycardia algorithm allowed confirmation of the appropriateness of permanent pacing in a majority of patients suffering from CSS. [source]