Gastrocardiac syndrome: A forgotten entity

Symptomatic bradycardia due to gastric distension is a rarely reported entity in the field of medicine. The mechanism of gastrointestinal distention that contributes to bradycardia is complex. A 75-year-old female with recurrent episodes of dizziness in the setting of gastric distension was found to have severe sinus bradycardia which resolved upon resolution of gastric distension. No structural or functional abnormality of heart was found. The patient was treated with permanent pacemaker implantation due to recurrent episodes of dizziness in the setting of sinus bradycardia.     

Temporary coronary sinus pacing to improve ventricular dyssynchrony with cardiogenic shock: A case report

BACKGROUNDTemporary transvenous pacing through the coronary sinus is a novel approach rarely used in treating unstable bradycardia. This modality could provide cardiac pacing while achieving better ventricular synchrony. We present a case who received cardiac pacing through the coronary sinus and provide a summary of evidence in the current literature.CASE SUMMARYA 55-year-old woman with a history of advanced heart failure was admitted to the rehabilitation ward after a recent stroke. During hospitalization, she had paroxysmal atrial fibrillation with rapid ventricular response resulting from fluid overload. While atrial fibrillation was spontaneously reversed to sinus rhythm after diuresis, she developed multiple episodes of polymorphic ventricular tachycardia along with sinus bradycardia and prolonged QTc interval. She became hypotensive despite appropriate medical management. Pacing through her implantable cardioverter-defibrillator was attempted but worsened her hypotension. Ventricular dyssynchrony was suspected. Temporary transvenous atrial pacing through the coronary sinus was performed, which stabilized her blood pressure and improved end-organ perfusion. A permanent biventricular pacemaker was later implanted, and she was safely discharged to a nursing home.CONCLUSIONTemporary transvenous pacing through the coronary sinus, a novel approach to treat unstable bradycardia, may reduce ventricular dyssynchrony.     

Clinical significance of intrinsic sympathomimetic activity of the beta blocker carteolol. II: Comparative studies of carteolol and pindolol in patients with bradycardia

Completing previous studies in patients with sinus bradycardia (Med. Klin. 82 [1987], 647-650) we compared metoprolol with carteolol and pindolol, pindolol with carteolol, no treatment with carteolol (in two groups) in five series of the paired comparisons of Holter-ECG each. With change from metoprolol to carteolol or pindolol (dose ratio 10:1) lowest heart rate on Holter-ECG increased by 28 or 29% without change of exercise heart rate. Direct comparison of pindolol and carteolol revealed a very similar heart rate profile, indicating equipotent beta blockade and ISA. In patients with previous beta blocker induced bradycardia, carteolol did not change a normal resting heart rate off treatment. However, in patients with spontaneous sinus bradycardia carteolol increased lowest heart rate (+14%, due to overriding ISA) and lowered exercise heart rate (-15%, due to overriding beta blockade). A beta blocker induced sinus bradycardia consistently improved with change of treatment to carteolol and pindolol. With caution carteolol and pindolol may also be used despite spontaneous sinus bradycardia.     

Natural History of Sinus Node Chronotropy in Paced Patients

The natural history of chronotropic incompetence is not clear. To assess this, we evaluated corrected sinus node recovery time (cSNRT) and sinus node chronotropy at rest and during exercise in two groups of syncopal patients with sinus node disease. Group A comprised patients with resting bradycardia but normal cSNRT and group B had resting bradycardia and prolonged cSNRT (> 1000 ms). An additional two groups (C and D) were studied. Group C comprised patients with complete AV (CAVB) and no evidence of sinus node disease and group D were asymptomatic controls of similar age. At diagnosis, patients with symptomatic bradycardia but normal cSNRT and no evidence of carotid sinus syndrome (group A) had resting bradycardia and impaired peak heart rate (PHR-I) on exercise compared to controls (P < 0.001 and P < 0.05, respectively), but no reduction in exercise duration. At follow-up group A patients demonstrated an increase in resting rate that was significantly slower than the controls (P < 0.01). Peak heart rate (PHR-II) also remained significantly slower (P < 0.05). There was no difference in exercise duration between groups A and D at follow-up. Group B was further subdivided according to follow-up findings of preservation of atrial activity in seven patients (group B-1) and junctional rhythm without any atrial activity in four patients (group B-2). Retrospective analysis showed no significant difference in resting heart rate at initial examination but group B-2 showed a significantly lower peak heart rate on exercise compared with B-1 (P < 0.01). Follow-up exercise tests revealed reduced exercise capacity in B-2 patients when compared with B-1 (P < 0.05) and both B-1 and B-2 had significantly reduced exercise capacity when compared with control groups C and D (P < 0.001). Group C patients had an initial sinus node chronotropic response to exercise, which was not different from control but significantly better (P < 0.01) than group B. At follow-up, the mean peak sinus rate of group C patients was unchanged, while there was an insignificant prolongation of cSNRT. Thus, patients with resting bradycardia, blunted peak heart rate response to exercise, and markedly prolonged CSNRT are those most likely to show chronotropic incompetence over the long-term and should be considered for rate responsive dual (or single) chamber pacing systems.     

Bradycardia and Syncope in Children Not Controlled by Pacing: Beta-Adrenergic Hypersensitivity

Cardiac pacing is frequently employed in the therapy of children with syncope and documented bradycardia. This report describes two children, ages 7 and 9 years, who underwent placement of demand ventricular pacing systems for documented bradycardia and syncope. Cardiac catheterization and intracardiac electrophysiological studies failed to show evidence of structural abnormalities, sinus node or conduction system disease, inducible arrhythmias, or VA conduction in each patient. Both patients had persistent symptoms after pacemaker implantation. Autonomic function testing with continuous heart rate and blood pressure monitoring revealed exaggerated beta-adrenergic responses to simple standing and small doses of isoproterenol. Symptoms were completely eliminated with atenolol. In these two children, cardiac pacing alone was not adequate for relief of symptoms. Autonomic mechanisms of bradycardia and hypotension should be considered prior to implantation of permanent pacing systems in children.     

Symptomatic sinus node disease: natural history after permanent ventricular pacing.

Fifty-nine patients between the ages of 13 and 88 with sinus node disease, who received a permanent ventricular pacemaker between 1965 and 1976 at one institution, were followed to determine the natural history of the disorder after permanent pacing. Nineteen had ischemic heart disease, six had primary myocardial disease, and eight valvular heart disease. In 26, no etiology for the arrhythmia was apparent. The one- and five-year survival was 85.5% and 73.1%, respectively. Patients with underlying heart disease had a significantly poorer survival when compared to those without (58% versus 94% at 36 months) and all but 3 of 13 deaths in the first 36 months were in those with ischemic heart disease. There was a distinct trend toward poor survival in those with heart failure prior to pacemaker implant and those over age 65. Patients with sinus bradycardia alone did best (91% survival three years after implant), while those with bradycardia-tachycardia syndrome and those with sinoatrial arrest alone did distinctly worse (76% and 65% survival at three years, respectively). Twelve of 18 deaths were due to progression of underlying heart disease. The long-term prognosis with symptomatic sinus node disease can be predicted in part by (1) etiology of the underlying heart disease, (2) pre-implant arrhythmia, and (3) ventricular function prior to implant.     

经导管消融治疗心房颤动伴心动过缓

目的探讨经导管消融治疗心房颤动合并心动过缓的方法和患者的安全性。方法对24例心房颤动伴心动过缓患者行经导管消融治疗心房颤动,消融策略包括环肺静脉电隔离、左心房线性消融及复杂心房碎裂电位(CFAE)消融。观察消融前及术后1个月动态心电图,并记录24h平均心率、最高窦性心率,以超声心动图评价术后6个月左心房直径变化。结果心房颤动消融术后患者平均心率、最高窦性心率均高于术前(P<0.001);术后6个月左心房舒张末期直径减小(P<0.001)。经(19.8±9.9)个月门诊随访,15例(15/24,62.50%)无心房颤动复发,无缓慢型心律失常相关症状;6例患者仍有房性期前收缩或房性心动过速发作,1例患者因心动过缓植入起搏器治疗,余2例心房颤动发作较术前频度减少。结论心房颤动转复时的窦性停搏和心动过缓以及部分快-慢综合征患者的窦房结功能不良可能是源于快速心房率对窦房结功能的抑制。对这部分患者行经导管消融治疗可安全、有效地改善窦房结功能不良,逆转重构。     

Thalidomide-induced sinus bradycardia

OBJECTIVE: To report a case of thalidomide-induced sinus bradycardia in an elderly man. CASE SUMMARY: A 72-year-old white man, with transfusion-dependent refractory anemia with ringed sideroblasts and hypertension treated with atenolol, was started on thalidomide 100 mg at bedtime. During the dose titration period (maximum dose 400 mg/d), his heart rate decreased from a baseline of 63 beats/min to as low as 44 beats/min with positive electrocardiogram findings of sinus bradycardia. After discontinuation of atenolol, the patient's heart rate increased to 68 beats/min, but symptoms of bradycardia persisted. Due to the patient's continued dizziness and lightheadedness, thalidomide was discontinued. In the 3 months following discontinuation of thalidomide, the patient's heart rate increased to an average of 74 beats/min. DISCUSSION: Clinical trials and postmarketing surveillance suggest that the incidence of thalidomide-induced bradycardia is low. The mechanism of this effect is unknown. Concurrent medications affecting the heart rate may also increase the risk of thalidomide-induced bradycardia. Following titration of thalidomide to a maximum dose of 400 mg/d, our patient's heart rate decreased markedly, resulting in intermittent symptoms of lightheadedness and dizziness. He may have been at higher risk of thalidomide-induced bradycardia because of concurrent administration of atenolol. An objective causality assessment revealed that the adverse event was probable. CONCLUSIONS: Despite the low incidence of thalidomide-induced bradycardia, it appears to be an important adverse effect, particularly in patients with comorbidities or concurrent medications that decrease heart rate. Therefore, providers should monitor these patients closely for signs and symptoms of bradycardia during the administration of thalidomide.     

Natural History of Severe Sinus Bradycardia Discovered by 24 Hour Holter Monitoring

This study follows patients with severe sinus bradycardia (40 beats per minute for 6 seconds or greater) in order to evaluate mortality and the effectiveness of permanent pacemaker insertion. Severe sinus bradycardia was noted on a 24-hour Holter in 95 patients. There were 64 males and 31 females with a mean age of 69 +/- 10 years. All were available for follow-up at 26 +/- 13 months. Twenty-eight required a permanent pacemaker at an average of 2 +/- 3 months after the Holter. Of this group 12 had the Holter for arrhythmia, 11 for cerebral symptoms, 4 for palpitations and 1 for chest pain. Only 1 was taking digitalis and no patients were taking Inderal. Six (21%) died at a mean interval of 21 +/- 15 months following pacemaker insertion. Sixty-seven did not require pacemaker insertion. The indications for Holter monitoring were arrhythmia in 16, palpitations in 19, cerebral symptoms in 20 and chest pain in 12. Four of these patients were on digitalis, 8 on Inderal, and 4 on both. Eleven (16%) died at a mean interval of 12 +/- 7 months after the initial Holter recording. Dizziness and/or syncope reoccurred in 22. Five had these symptoms even after pacemaker insertion. We conclude that severe sinus bradycardia is associated with a significant mortality. Insertion of a permanent pacemaker may decrease recurrent symptoms and slightly increase time of survival, but does not appear to influence the overall survival rate.     

Electrophysiologic Properties of Cimetidine in Man

Severe bradycardia has been reported with the use of cimetidine. This observation has been explained by histamines' known action in increasing the contraction rate of the spontaneously beating right atrium, strips of ventricular muscle, and whole heart of guinea pigs. Histamine can also produce cardiac arrhythmias in animals. There is evidence for H2 receptors in the heart. Black and his associates have shown that the characteristic effect of histamine on isolated guinea pig atrium could be selectively blocked by anti-H2 drugs. Thus cimetidine probably can produce a sinus bradycardia by blocking the H2-receptor site in the heart. Recently Engel and Luck reported that 300 mgs of intravenously administered cimetidine did not affect heart rate, sinus node recovery time, or sinoatrial conduction time. These workers concluded that there is insufficient evidence to demonstrate that cimetidine caused appreciable sinus node dysfunction in man. In view of the disparity in these reports, we investigated the effects of 300 mgs of intravenously administered cimetidine on the human conduction system.     

Atrial Standstill: An Indication For Rate Responsive Pacing

Atrial standstill (atrial paralysis) is a rare reason for permanent bradycardia. A case of atrial standstill is presented. A 35-year-old man had suffered from bradycardia since his childhood. For 2 years he had complaints (diminishment of his working capacity, and dyspnea occurred with effort) as well. On admission, a slow (38/min) junctional escape rhythm could be detected. There were no signs of atrial mechanical activity (atrial contraction) according to chest x ray, echocardiography, and the atrial pressure curve. The electrophysiological study revealed that the atria could not be electrically stimulated, and no P wave (A wave) could be recorded on right atrial electrograms. The patient received a rate responsive pacemaker. After pacemaker implantation, he became symptom-free; his working capacity improved markedly and his heart size decreased. Owing to the permanent bradycardia and the lack of atrial stimulation, the atrial standstill represents an indication for ventricular rate responsive pacing. Atrial standstill, permanent bradycardia, and the inability to stimulate the atrium are indications for ventricular rate responsive pacing.     

围术期心理干预对减轻胸交感神经切断术后代偿性多汗的意义

目的探讨围术期心理干预对减轻胸交感神经切断术后严重代偿性多汗的效果。方法分析2007年7月至2012年8月253例成功手术的因手多汗症行胸交感神经切断术患者,比较切断T3或T4不同平面胸交感神经及围术期心理干预后,代偿性多汗严重程度的发生率。结果 143例未进行特殊心理干预的手术患者,T3手术平面患者术后重度代偿性多汗发生率为15.15%(10/66),T4手术平面为9.1%(7/77),差异有统计学意义(P0.01)。110例经心理干预的患者手术后均未出现重度代偿性多汗,未进行心理干预的143例手术患者术后总的重度代偿性多汗发病率为11.89%(17/143),两组比较差异有统计学意义(P0.01)。结论围术期的心理干预可以从心理方面避免及克服患者对出汗的焦虑,对减轻术后严重代偿性多汗有显著效果。     

Combination of slow-release diltiazem and a beta-blocker in arterial hypertension. 2 cases of cardiogenic shock with severe bradycardia

Patient 1 received carteolol and captopril for hypertension. Three days after a slow-release diltiazem preparation (300 mg) had been introduced, he developed cardiogenic shock and sinus bradycardia (heart rate: 30/mn) with acidosis and severe hyperkaliemia. He was successfully treated by temporary pacing and dobutamine. Patient 2 had received sotalol and captopril for several years. Twelve hours after slow release diltiazem had been added, he was found in cardiogenic shock and extreme bradycardia with wide QRS, acidosis and hyperkaliemia. He died one hour later despite intensive emergency treatment. Concomitant use of beta-blockers and calcium channel blockers has been reported in patients suffering of severe coronary heart disease. However, several adverse reactions similar to our cases have been described. Slow-release diltiazem should be avoided in hypertensive patients taking beta-blockers.     

Dissection of carotid sinus hypersensitivity: the timing of vagal and vasodepressor effects and the effect of body position

We assessed the timing of vagal and sympathetic factors that mediate hypotension during CSM (carotid sinus massage) in patients with carotid sinus hypersensitivity. We hypothesized that a fall in cardiac output would precede vasodepression, and that vasodepression would be exaggerated by head-up tilt. We performed pulse contour analyses on blood pressure recordings during CSM in syncope patients during supine rest and head-up tilt. In a subset we simultaneously recorded muscle sympathetic nerve activity supine. During supine rest, systolic blood pressure decreased from 150±7 to 107±7 mmHg (P<0.001) and heart rate from 64±2 to 39±3 beats/min (P<0.01). Cardiac output decreased with heart rate to nadir (66±6% of baseline), 3.1±0.4?s after onset of bradycardia. In contrast, total peripheral resistance reached nadir (77±3% of baseline) after 11±1?s. During head-up-tilt, systolic blood pressure fell from 149±10 to 90±11 mmHg and heart rate decreased from 73±4 to 60±7 beats/min. Compared with supine rest, cardiac output nadir was lower (60±8 compared with 83±4%, P<0.05), whereas total peripheral resistance nadir was similar (81±6 compared with 80±3%). The time to nadir from the onset of bradycardia did not differ from supine rest. At the onset of bradycardia there was an immediate withdrawal of muscle-sympathetic nerve activity while total peripheral resistance decay occurred much later (6-8?s). The haemodynamic changes following CSM have a distinct temporal pattern that is characterized by an initial fall in cardiac output (driven by heart rate), followed by a later fall in total peripheral resistance, even though sympathetic withdrawal is immediate. This pattern is independent of body position.     

Long-Term Intrinsic Pacemaker Function in Patients Paced for Sinus Node Deficiency After Cardiac Transplantation

Fifteen cardiac transplant recipients requiring permanent pacing (AAJ, n = 9; VVI, n = 6; rate responsive devices, n = 11) for postoperative sinus node (SN) insufficiency underwent evaluation of long-term SN function 240 to 1,461 days after transplantation. The intrinsic rhythm at the time of discharge was sinus in 7 patients; functional escape in 6 patients; and pacemaker dependent in 2 patients. At follow-up, 5 patients had regained regular sinus rhythm, accounting for a total of 11 patients in sinus rhythm while 4 patients were in functional bradycardia. The SN recovery time as determined by the permanent pacemaker was normal (< 1,500 msec) in only 1/8 patients in whom it was determined, although 4 of these 8 patients were temporarily overriding the pacemaker during ambulatory monitoring. Patients with pathological SN recovery times included 3 patients with late return of sinus rhythm and 4 patients who had recovered normal sinus rhythm before their discharge from the hospital. Three patients developed late symptoms despite apparent early normalization and underwent delayed pacemaker implantations on postoperative days 35, 52, and 225, respectively. We conclude that, in patients requiring pacemaker implantation after cardiac transplantation, normalization of SN function cannot be inferred from just return of sinus rhythm, regardless of whether it occurs early or late. These findings may have implications when a pacemaker exchange or explanation is being considered.     

The Contribution of HCN4 to Normal Sinus Node Function in Humans and Animal Models

Although sinus node bradycardia is a very common clinical condition, the cellular mechanisms contributing to abnormal sinus node function are not clearly delineated. In recent publications, mutations in the hyperpolarization-activated, cyclic nucleotide-gated (HCN) 4 channels have been associated with sinus bradycardia. These channels are thought to be crucial in generating the spontaneous sinus node action potential, in accelerating the heart rate during sympathetic drive, and decelerating heart rate during vagal stimulation. Humans carrying HCN4 mutations indeed display significant bradycardia. Recent studies generating HCN4 knock out mice suggested that although HCN4 is crucial in early development, other mechanisms may also play a role in the accelerated heat rate achieved during sympathetic drive. In this review, we focus on genotype–phenotype correlation of these mutations and discuss the relative contribution of various ion channels to sinus node function. We also discuss the importance of HCN in treating clinical conditions such as brady- and tachycardia. (PACE 2010; 100–106)     

心动过缓伴ST段压低在病窦综合征诊断中的价值

目的：对心动过缓伴ST段压低的现象进行讨论，评估其在病窦综合征诊断中的价值。方法：31例患者行窦房结功能评估、踏车试验、冠状动脉造影和药物试验。结果：26例完成全部研究，其中，11例判定为病窦综合征，15例窦房结功能正常。两组踏车试验中均有部分患者出现心率反应不良，其冠状动脉造影特征为病变均涉及右冠和／或回旋支，而心率反应正常者多为单纯前降支病变；后者进入药物试验，均观察到慢频率依赖性sT段压低。结论：心动过缓与ST段压低可互为因果，并对窦房结功能是否可逆、病因是否属缺血性有诊断价值。     

Hemodynamic pharmacology of p-chloroamphetamine, a serotonin agonist, in conscious rats

The hemodynamic effects of p-chloroamphetamine (PCA), an indirect serotonin (5-HT) agonist, were studied in conscious, unrestrained rats. PCA caused an immediate hypotension and bradycardia followed by a dose-dependent increase in mean arterial pressure (MAP), which lasted for 15 to 60 min, associated with variable effects on heart rate. An intermediate dose increased MAP and resistance in hindquarter and mesenteric, but not renal, vascular beds. The pressor effect of PCA was blocked by prazosin and by 6-hydroxydopamine plus adrenal demedullation, but not by 6-hydroxydopamine or adrenal demedullation separately. Ganglionic blockade with chlorisondamine or beta adrenoceptor blockade with propranolol potentiated the pressor response to PCA, whereas several manipulations of central 5-HT systems (fluoxetine, methysergide and 5,7-dihydroxytryptamine) reduced but did not eliminate the hypertension observed after PCA. The initial bradycardia and hypotension were abolished by chlorisondamine or atropine but not reduced by any other pretreatment, whereas the variable heart rate response was converted to a marked, sustained tachycardia by ganglionic blockade or atropine and to a consistent bradycardia by propranolol and peripheral sympathectomy. The data suggest that PCA causes an immediate central or reflex vagal activation to decrease heart rate and MAP, followed by a central 5-HT-mediated increase in sympathetic activity that increases MAP. Most of the pressor effect observed between 5 and 30 min after PCA appears to be mediated by a direct effect on release of norepinephrine and epinephrine from sympathetic nerve terminals and the adrenal medulla, respectively. Only a minor part of the hemodynamic response to PCA appears to be attributable to its effect on release of 5-HT in the brain.     

胸腔镜下交感神经切除对血流动力学的影响

目的观察电视胸腔镜(video assisted thoracoscopic surgery，VATS)下胸交感神经切除术(transthoracic endoscopic sympathectomy，TES)时CO2人工气胸及手术操作对血流动力学的影响。方法对35例手汗症患者在气管插管全身麻醉情况下行胸腔镜下双侧胸交感神经切除。术中给予3～5cmH2O的CO2胸腔正压。观察记录患者麻醉前、诱导后、手术开始时、先后两侧胸交感神经切除时、胸交感神经切断后5min、10min心率(HR)、收缩压(SBP)、舒张压(DBP)、平均压(MAP)、中心静脉压(Cvp)、经皮氧饱和度(SpO2)变化。结果与麻醉前及手术开始时相比，术中HR明显减慢；与麻醉前相比，诱导后SBP、DBP、MAP明显下降，手术开始及以后各时点SBP、DBP、MAP平稳；CVP和SpO2平稳。结论在行胸腔镜下交感神经切除时。特别是在交感神经切断后能引起心率减慢。在3～5cmH2的CO2胸腔正压下行TES能在保证手术视野和操作的情况下将SBP、DBP、MAP、SpO2维持在正常范围。     

Intravenous theophylline--an alternative to temporary pacing in the management of bradycardia secondary to AV nodal block

OBJECTIVE: To report a case of bradycardia secondary to atrioventricular nodal block (AVNB) successfully treated with intravenous theophylline. Intravenous theophylline was used as an alternative to temporary pacing in a patient with sepsis secondary to thermal injury. CASE SUMMARY: A 79-year-old white woman with significant cardiac history was admitted with 14.5% total body surface area burns after a house fire. Cardiac events included intermittent episodes of sinus bradycardia complicated by the development of second-degree AVNB and periods of sinus arrest. Intravenous theophylline initiation maintained normal sinus rhythm without further episodes of sinus bradycardia or heart block, thus preventing the need for cardiac pacemaker placement. DISCUSSION: This is the first case published in the English-language literature describing the use of intravenous theophylline as an alternative therapy to temporary pacing in a patient with sepsis secondary to thermal injury. Bradyarrhythmic events in sepsis patients have been associated with catecholamine production increasing adenosine formation. High concentrations of adenosine in the areas of the sinoatrial or atrioventricular nodal regions may induce sinus bradycardia or AVNB. Theophylline, an adenosine antagonist, has been identified as a treatment option for such bradyarrhythmic events. CONCLUSIONS: Theophylline, a methylxanthine derivative, may represent an alternative to other pharmacologic therapies and temporary pacing in the treatment of bradycardia secondary to AVNB. These agents may represent a pharmacologic alternative in patients in whom other pharmacologic strategies or cardiac pacemaker insertion may be contraindicated.