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Sinus Syndrome (sinus + syndrome)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Sinus Syndrome

  • carotid sinus syndrome
    		•
  • sick sinus syndrome
    		•

    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]

    Predictors of Failure to Cure Atrial Fibrillation with the Mini-Maze Operation

    JOURNAL OF CARDIAC SURGERY, Issue 1 2004
    Zoltan A. Szalay M.D.
    A reduction in the number of right and left atrial incisions could decrease the operative time. The aim of this study was to assess the results of a mini-maze operation and to define predictors of its failure. Methods: Between 1995 and 2000, 72 patients (mean age 64 ± 9 years) undergoing cardiac surgery had a concomitant mini-maze operation for symptomatic chronic atrial fibrillation. Three and 12 months postoperatively, heart rhythm and left atrial transport functions were assessed by electrophysiology, echocardiography, and magnetic resonance imaging. Multivariate analysis was performed to identify predictors of failure of the mini-maze operation. Results: Operative mortality was 1.4% (1/72). Death during follow-up occurred in 5.6% of patients (4/71), in one due to chronic heart failure. After 1 year, 80% of patients (48/60) were either in sinus rhythm (n = 43; 72%) or had a pacemaker (n = 5; 8%) implanted due to sick sinus syndrome. Intermittent and chronic atrial fibrillation was found in 20% of patients (12/60). Preoperative duration of atrial fibrillation (p = 0.05), preoperative left atrial diameter (p = 0.001), preoperative right atrial diameter (p = 0.02), a reduced left ventricular ejection fraction (p = 0.03), an increased left ventricular end-diastolic diameter (p = 0.04), and the presence of mitral valve stenosis (p = 0.001) were found to be univariate predictors of failure of the mini-maze operation 1 year postoperatively. Multivariate analysis defined preoperative diagnosis of mitral valve stenosis (p = 0.005; OR 117.5), longer duration of preoperative atrial fibrillation (p = 0.01; OR 1.33), and increased preoperative left ventricular end-systolic diameter (p = 0.02; OR 1.2) as incremental independent risk factors for failure of the mini-maze operation to cure chronic atrial fibrillation. Conclusion: The mini-maze operation is a safe procedure with similar results to that of Cox's Maze-III operation. The less-invasive mini-maze operation could be applicable even to patients with severely reduced left ventricular function, in whom complex cardiac surgery has to be performed concomitantly as well as in those presenting severe comorbidities. (J Card Surg 2004;19:1-6) [source]

    Sudden Cardiac Death and Inherited Arrhythmia Syndromes

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005
    ANDREA SARKOZY M.D.
    Sudden cardiac death (SCD) at youth is rare and is often caused by inherited cardiac disorders. This review focuses on the genetic background of inherited primary electrical diseases, the so-called "channelopathies." Following a short clinical description of each syndrome, the recent findings in the genetics of long QT syndrome, short QT syndrome, isolated cardiac conduction defect, familial sick sinus syndrome, familial atrial fibrillation, cathecholaminergic polymorphic ventricular tachycardia, familial Wolff-Parkinson-White (WPW) syndrome, and Brugada syndrome are discussed. The currently proposed theoretical model of overlapping phenotypes in SCN5A sodium channel mutations is presented. The recent data indicate that advances in molecular genetics, experimental and clinical electrophysiology shed some light on the genetic background of primary electrical diseases. However, it is also becoming clear that the process from a mutation of a gene to the clinical presentation of a patient is currently only partially understood and extremely complex. [source]

    Cerebral and Oculorhinal Manifestations of a Limited Form of Wegener's Granulomatosis With c-ANCA,Associated Vasculitis

    JOURNAL OF NEUROIMAGING, Issue 1 2001
    Peterus Thajeb MD
    ABSTRACT The authors report on cerebral and oculorhinal manifestations in a patient with a cytoplasmic pattern of antineutrophil cytoplasmic autoantibody (c-ANCA),associated vasculitis. Recurrent Tolosa-Hunt syndrome, cavernous sinus syndrome, Raeder's paratrigeminal neuralgia, and seizures were the major clinical manifestations. Brain MRI showed localized enhancing lesions initially in the cavernous sinus and later in the convexity pachymeninges. The lesions disappeared following 9 months of oral prednisolone (15 mg/day) and cyclophosphamide (100 mg/day) therapy. The presence of c-ANCA, demonstration of vasculitis, and depositions of immunoglobulin G (IgG) and fibrinogen in the vessel walls of pachymeninges of the patient confirmed an immune-mediated cause of the vasculitis. Cranial pathology without renal and pulmonary involvement suggests a variant of Wegener's granulomatosis, which is called the "limited" form of Wegener's granulomatosis. [source]

    Results of pacemaker implantation in 104 dogs

    JOURNAL OF SMALL ANIMAL PRACTICE, Issue 1 2007
    M. S. Johnson
    Objectives: To document the outcome, survival and complications involved in pacemaker implantation in dogs in a retrospective study. Methods: Case records for all dogs in which pacemaker implantation was performed were reviewed. Results: A total of 104 dogs underwent pacemaker implantation. Dogs were presented with atrioventricular (AV) block (71), sick sinus syndrome (25) or vasovagal syncope (eight). Age at presentation varied from six months to 13 years with a median age of seven years and two months. The Labrador was the most commonly represented breed (17 cases). All but one dog survived pacemaker implantation, with 93 showing resolution of their clinical signs while 10 dogs showed intermittent residual signs. One-, three- and five-year survival estimates were 86, 65 and 39 per cent, respectively. Major complications after implantation were documented in 15 dogs and three of these led to fatalities. Minor complications were noted in 23 dogs. Sudden death occurred in six dogs three to 55 months following successful pacemaker implantation. Clinical Significance: Transvenous pacemaker implantation was successful in reducing or eliminating clinical signs in over 90 per cent of dogs with third-degree atrioventricular (AV) block or sick sinus syndrome. In dogs with vasovagal syncope, six of eight dogs had greatly reduced frequency of collapse and two became asymptomatic. Although the procedure was associated with complications, these were rarely life threatening and good survival was documented in the majority of cases. [source]

    Effect of Right Ventricular Apex Pacing on the Tei Index and Brain Natriuretic Peptide in Patients with a Dual-Chamber Pacemaker

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2006
    HITOSHI ICHIKI
    Background: Asynchronous electrical activation induced by right ventricular apex (RVA) pacing can cause various abnormalities in left ventricular (LV) function, particularly in the context of severe LV dysfunction or structural heart disease. However, the effect of RVA pacing in patients with normal LV and right ventricular (RV) function has not been fully elucidated. The aim of this study was to characterize the effects of RVA pacing on LV and RV function by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time (Tei index) and by assessing changes in plasma brain natriuretic peptide (BNP). Methods: Doppler echocardiographic study and BNP measurements were performed at follow-up (mean intervals from pacemaker implantation, 44 ± 75 months) in 76 patients with dual chamber pacemakers (sick sinus syndrome, n = 30; atrioventricular block, n = 46) without structural heart disease. Patients were classified based on frequency of RVA pacing, as determined by 24-hour ambulatory electrocardiogram (ECG) that was recorded just before echocardiographic study: pacing group, n = 46 patients with RVA pacing ,50% of the time, percentage of ventricular paced 100 ± 2%; sensing group, n = 30, patients with RVA pacing <50% of the time, percentage of ventricular paced 3 ± 6%. Results: There was no significant difference in mean heart rate derived from 24-hour ambulatory ECG recordings when comparing the two groups (66 ± 11 bpm vs 69 ± 8 bpm). LV Tei index was significantly higher in pacing group than in sensing group (0.67 ± 0.17 vs 0.45 ± 0.09, P < 0.0001), and the RV Tei index was significantly higher in pacing group than in sensing group (0.34 ± 0.19 vs 0.25 ± 0.09, P = 0.011). Furthermore, BNP levels were significantly higher in pacing group than in sensing group (40 ± 47 pg/mL vs 18 ± 11 pg/mL, P = 0.017). With the exception of LV diastolic dimension (49 ± 5 mm vs 45 ± 5 mm, P = 0.012), there were no significant differences in other echocardiographic parameters, including left atrium (LA) diameter (35 ± 8 mm vs 34 ±5 mm), LA volume (51 ± 27 cm3 vs 40 ± 21 cm3), LV systolic dimension (30 ± 6 mm vs 29 ± 7 mm), or ejection fraction (66 ± 9% vs 63 ± 11%), when comparing the two groups. Conclusions: These findings suggest that the increase of LV and RV Tei index, LVDd, and BNP are highly correlated with the frequency of the RVA pacing in patients with dual chamber pacemakers. [source]

    Pacemaker Lead Endocarditis Caused by Staphylococcus Hominis

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2006
    MUSTAFA SUNBUL
    Infective endocarditis related to pacemaker is a rare but serious condition in permanent venous tracing. A 65-year-old man was admitted to the hospital with high fever and chills. A DDD pacemaker had been implanted via the right subclavian vein because of sick sinus syndrome 6 years earlier. Transesophageal echocardiogram identified an oscillating round hyperechoic mass with a stalk near the tricuspid valve. Blood cultures grew Staphylococcus hominis. The patient was treated with antibiotics and operated on after the acute phase of the illness had subsided. We hereby report a case of lead endocarditis caused by S. hominis in a patient with pacemaker, which has been rarely reported in the English literature. [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]

    Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing Rate

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000
    IVAN ILIEV ILIEV
    The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source]

    Effects of theophylline on exercise indices in a patient with chronotropic incompetence

    CLINICAL CARDIOLOGY, Issue 10 2000
    William C. Dixoniv M.D.
    Abstract Several investigators have documented the successful use of oral sustained-release theophylline in treating symptomatic bradycardia and sick sinus syndrome. This paper reports a case of chronotropic incompetence in which specific exercise indices, including the chronotropic response index, were used to measure the therapeutic efficacy of theophylline. [source]

    Ageing to arrhythmias: conundrums of connections in the ageing heart

    JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 12 2006
    Sandra A. Jones
    The proportion of the population that is elderly continues to increase, leading to an increasing need to address problems chiefly associated with old age. Progressive ageing of the heart is associated with an increasing incidence of arrhythmias and disorders of the normal origin of the heartbeat, the sinoatrial node. This intrinsic pacemaker of the heart has an increasing tendency with age to lose its dominant role in pacing the heart, and regulation of heart rate becomes erratic. This ,sick sinus syndrome' is associated with fainting, palpitations, shortness of breath and sudden death. Current treatment of this condition is by implantation of an artificial pacemaker, an intervention increasingly required with age. The current evidence suggests that the normal heartbeat fails due to changes in the expression of critical proteins that ensure the correct production and conduction of the cardiac action potential. Depletion of a protein directly responsible for providing electrical connections between the cells of the heart, connexin 43, appears to leave the normal cardiac pacemaker disconnected and unable to drive the heart. This process may be associated with age-dependent changes in stress-related signalling. Simple interventions such as exercise could impact on the processes hypothesized to be involved and may offer a means to preserve the stability of the electrical activity of the heart into old age without pharmacological manipulation. [source]