Sinus Node Dysfunction due to Occlusion of the Sinus Node Artery during Percutaneous Coronary Intervention.

BACKGROUND: Sinus node artery occlusion (SNO) is a rare complication of percutaneous coronary intervention (PCI). We analyze both the short- and long-term consequences of SNO. METHODS: We retrospectively reviewed 1379 consecutive PCI's involving RCA and Cx arteries performed in our heart institute from 2016 to 2019. Median follow-up was 44 ± 5 months. RESULTS: Among the 4844 PCIs performed during the study period, 284 involved the RCA and the circumflex's proximal segment. Periprocedural SNO was estimated by angiography observed in 15 patients (5.3%), all originated from RCA. The majority of SNO occurred during urgent and primary PCIs following acute coronary syndrome (ACS). Sinus node dysfunction (SND) appeared in 12 (80%) of patients. Four (26.6%) patients had sinus bradycardia, which resolved spontaneously, and 8 (53.3%) patients had sinus arrest with an escaped nodal rhythm, which mostly responded to medical treatment during the first 24 hours. There was no association between PCI technique and outcome. Three patients (20%) required urgent temporary ventricular pacing. One patient had permanent pacemaker implantation. Pacemaker interrogation during follow-up revealed a recovery of the sinus node function after one month. CONCLUSION: SNO is rare and seen mostly during angioplasty to the proximal segment of the RCA during ACS. The risk of developing sinus node dysfunction following SNO is high. SND usually appears during the first 24 h of PCI. The majority of SND patients responded to medical treatment, and only in rare cases were permanent pacemakers required.

Electrical isolation of the superior vena cava using second-generation cryoballoon in patients with atrial fibrillation.

BACKGROUND: The safety and efficacy of superior vena cava (SVC) isolation using second-generation cryoballoon (CB) ablation remain unknown. METHODS: A total of 26 (3.2%) patients with SVC-related paroxysmal atrial fibrillation (AF) from a consecutive series of 806 patients who underwent second-generation CB were included. Pulmonary vein isolation was initially achieved by CB ablation. If the SVC trigger was determined, the electrical isolation of SVC isolation was performed using the second-generation CB. RESULTS: Real-time SVC potential was observed in all patients. Isolation of the SVC was successfully accomplished in 21 (80.8%) patients. The mean number of freeze cycles in each patient was 2.1 ± 1.1. The mean time to isolation and ablation duration were 22.5 ± 14.2 seconds and 94.5 ± 22.3 seconds, respectively. A transient phrenic nerve (PN) injury was observed in five patients (19.2%). There were two patients (7.7%) experienced reversible sinus node injury during the first application. During a mean follow-up period of 13.2 ± 5.8 months, four patients (15.4%) had atrial arrhythmia recurrences. CONCLUSION: Isolation of SVC using the second-generation 28-mm CB is feasible when SVC driver during AF is identified. Vigilant monitoring of PN function during CB ablation of SVC is needed to avoid PN injury.

We Know What the Cardiac Surgeon Did During Last Hybrid Arrhythmia Procedure.

Superior vena cava (SVC) is an important source of origin of atrial fibrillation (AF) triggers other than a pulmonary vein. Because of the proximity of SVC-aorta ganglionic plexi to the SVC and the extension of myocardium in the SVC from the right atrium, SVC frequently becomes an important source of ectopic beats initiating AF. The potential complications of SVC isolation may include sinus node injury. Sinus node isolation was observed in a patient who had undergone previous surgical isolation of SVC for AF, while attempting to ablate endocardially, near the superior part of interatrial septum for an atrial tachycardia.

Sinus node injury as a result of superior vena cava isolation during catheter ablation for atrial fibrillation and atrial flutter.

BACKGROUND: The ectopic foci originating from superior vena cava (SVC) may act as triggers in the occurrence and perpetuation of atrial fibrillation (AF). Unfortunately, the SVC isolation may result in potential dysfunction of sinus node. Furthermore, little is known about the occurrence of sinus node injury complicated by the SVC isolation. METHODS: Patients with AF or atypical atrial flutter experienced SVC isolation. The junctional rhythm or sinus arrest could be observed, if sinus node was injured. Atropin and dopamine administration ruled out the vagal irritation of sinus node, when junctional rhythm or sinus arrest occurred. RESULTS: One hundred and thirty-two patients who had no electrocardiogram signs of sinus node dysfunction before ablation experienced the SVC isolation. Six patients (three men, three women, mean age 62.5 ± 8.6 years) had sinus node injury (4.5%, 6/132): four patients had junctional rhythm and one male patient had junctional rhythm and sinus arrest simultaneously; another male patient required AAI mode permanent pacemaker implantation due to the persistent junctional rhythm after SVC isolation. The ablation sites of all six patients closed to the junction of right atrium and SVC during the ablation of anterolateral free wall of the SVC. CONCLUSION: Sinus node may be damaged due to the ablation sites closer to sinus node. The definition of the junction of right atrium and SVC is very important, the ablation sites of anterolateral free wall of the SVC should not be too close to the SVC orifice.

Sinus node injury as a complication of superior vena cava isolation.

We report a case with SVC ectopy initiating AF; the origin and breakout point of the sinus node was inside the SVC, and the SVC ectopy was conducted through the same path as the sinus node activation to depolarize the right atrium. Injury to the sinus node happened after successful isolation of SVC.

Exaggerated cardiovascular effects of cocaine in conscious dogs with pacing-induced dilated cardiomyopathy.

BACKGROUND: The aim of this study was to explore the characteristics and mechanisms of the cardiovascular effects of cocaine in dilated cardiomyopathy. METHODS AND RESULTS: We studied the cardiovascular responses to acute intravenous cocaine (1 mg/kg) in 8 conscious, chronically instrumented dogs before and after the development of dilated cardiomyopathy induced by rapid ventricular pacing. To help elucidate the role of altered baroreflex function in mediating the cardiovascular effects of cocaine, we also studied responses in 3 conscious, chronically instrumented dogs that had undergone surgical sinoaortic baroreceptor denervation. Cocaine produced greater increases in heart rate (+57 +/- 8% from 112 +/- 5 beats/min versus +28 +/- 3% from 100 +/- 4 beats/min; P <.01), first derivative of left ventricular pressure (+30 +/- 5% from 1,714 +/- 147 mm Hg/sec versus +15 +/- 3% from 3,032 +/- 199 mm Hg/sec; P <.01), coronary vascular resistance (+28 +/- 5% from 2.3 +/- 0.3 mm Hg/mL/min versus +11 +/- 5% from 2.2 +/- 0.3 mm Hg/mL/min; P <.05) and plasma norepinephrine concentration (+130 +/- 31% from 462 +/- 102 pg/mL versus +86 +/- 32% from 286 +/- 77 pg/mL; P <.05) in dogs with dilated cardiomyopathy as compared to controls. In addition, responses were much more rapid in onset following the development of dilated cardiomyopathy. Chronotropic and inotropic responses to cocaine were similarly rapid and exaggerated in dogs after baroreceptor denervation. CONCLUSIONS: Cocaine produces rapid and exaggerated chronotropic, inotropic, and coronary vasoconstrictor responses in conscious dogs with pacing-induced dilated cardiomyopathy. Alterations in arterial baroreflex function may play a role in these observations, which in turn may underlie the clinically observed association between cocaine and heart failure.

Sinus nodal function and risk for atrial fibrillation after coronary artery bypass graft surgery.

BACKGROUND: Nonsurgical patients with sinus node dysfunction are at high risk for atrial tachyarrhythmias, but whether a similar relation exists for atrial fibrillation after coronary artery bypass graft surgery is not clear. The purpose of this study was to evaluate sinus nodal function before and after coronary artery bypass graft surgery and to evaluate its relation with the risk for postoperative atrial arrhythmias. METHODS: Sixty patients without complications having elective coronary artery bypass graft surgery underwent sinus nodal function testing by measurement of sinoatrial conduction time (SACT) and corrected sinus nodal recovery time (CSNRT). Patients were categorized based on whether postoperative atrial fibrillation developed. RESULTS: Twenty patients developed atrial fibrillation between postoperative days 1 through 3. For patients remaining in sinus rhythm (n = 40), sinoatrial conduction times were no different and corrected sinus nodal recovery times were shorter after surgery when compared with measurements obtained after anesthesia induction. Sinus node function test results before surgery were similar between the sinus rhythm and the atrial fibrillation groups. After surgery, patients who later developed atrial fibrillation had longer sinoatrial conduction times compared with the sinus rhythm group (P = 0.006), but corrected sinus nodal recover time was not different between these groups. A sinoatrial conduction time > 96 ms measured at this time point was associated with a 7.3-fold increased risk of postoperative atrial fibrillation (sensitivity, 62%; specificity, 81%; positive and negative predictive values, 56% and 85%, respectively; area under the receiver operator characteristic curve, 0.72). CONCLUSIONS: These data show that sinus nodal function is not adversely affected by uncomplicated coronary artery bypass surgery. Patients who later developed atrial fibrillation, however, had prolonged sinoatrial conduction immediately after surgery compared with patients remaining in sinus rhythm. These results suggest that injury to atrial conduction tissue at the time of surgery predisposes to postoperative atrial fibrillation and that assessment of sinoatrial conduction times could provide a means of identifying patients at high risk for postoperative atrial fibrillation.

Long-term follow-up of dysrhythmias following the Mustard procedure.

Earlier reports have suggested that the incidence of dysrhythmias after the Mustard procedure can be reduced if the sinoatrial node (SAN) is protected during surgery. To determine if these initial differences continue after longer follow-up, we examined all ECGs available for three groups of patients operated upon from January, 1965, through December, 1977. Group A included 37 patients who survived the operation prior to January, 1972, when surgical modifications were initiated to protect the SAN; group B included 44 patients available for follow-up who were operated upon from 1972 through 1974; and group C consisted of the 39 patients available for follow-up operated upon from 1975 to 1977. Dysrhythmias were classified as passive (failure of initiation or propagation of the SAN impulse), active (atrial flutter or supraventricular tachycardia), or atrioventricular (AV) conduction defects. Results were expressed as the incidence per number of different rhythms during follow-up intervals. The incidence of sinus rhythm in groups B and C (80%) was much greater than in group A (27%) during the first 2 years. However, after 8 years, less than 50% of the rhythms were sinus. Both brady- and tachydysrhythmias were common. Seven patients (6%) required pacemaker insertion for symptomatic sick sinus syndrome. Therefore despite efforts to protect the sinus node, late occurring dysrhythmias remain a significant problem in the postoperative Mustard patient.

[Intraoperative electrophysiological localization of the origin of sinoatrial activity and examination of the location of the sinus node using microscope anatomic studies. Animal experiment study]. / Intraoperative elektrophysiologische Lagebestimmung des sinuatrialen Erregungsursprungs und Uberprüfung der Lage des Sinusknotens durch mikroskopisch-anatomische Untersuchung. Eine tierexperimentelle Studie.

Many electrophysiological and histological investigations have demonstrated that post-operative dysrhythmias which occur in children with heart disorders requiring extensive surgical treatment in the area of the right atrium, are often caused by intraoperative lesions of the sinoatrial node. Accordingly, accurate determination of that epicardial area which is closest to the primary pacemaking area of the sinoatrial node could prevent injuries and, thus, reduce the risk of postoperative arrhythmias. To localize the relevant area we developed a method which is based on the mapping technique in a series of experiments in dogs. The electrophysiological results were confirmed by histological or gross anatomical methods. After right lateral thoracotomy in the fifth intercostal space, the epicardial surface of the right atrium is subdivided into numbered fields by means of an imaginary grid. The local electrical activities are recorded as bipolar electrograms with the aid of two tripolar electrode probes, one fixed on the epicardium of the right atrial appendage and one placed onto the individual grid fields by the investigator. Intervals thus occur between those potentials derived from the mobile electrode probe and those derived from the fixed probe. Electrical activity originating from the sinoatrial node arrives earlier at the individual fields lying closer to the node than at the field of the fixed probe at the atrial appendage. Thus, the individual field associated with the longest interval between probe potentials must lie closest to the sinoatrial node. An electronic device with digital display of the interval length has been developed which enables, within three minutes, determination of the individual field with the longest interval. Comparison of the digital values with those measured from the electrograms shows good agreement. The experiments were carried out on eleven sheep dogs and large mongrels. In seven cases the location of the sinoatrial node was determined by subsequent histological examination. The assumption that the area associated with the longest interval between the probe potentials lies closest to the primary pacemaking region of the sinus node could be confirmed, since in all these cases the cranial portion of the sinoatrial node was located in the field with the greatest interval measured. In the other four cases the sinoatrial node was localized by dissection with the aid of a stereomicroscope. In three of the four cases, the cranial part of the sinoatrial node was also situated in the field associated with the longest interval.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias in transposition of the great arteries after the Mustard operation.

Disorders of rhythm or conduction in patients with transposition of the great arteries (TGA) after the Mustard operation have been widely reported. This study provides a systematic evaluation of the electrophysiologic function of 87 survivors of the Mustard operation at a single institution. Surface electrocardiograms were reviewed in all 87 patients, Holter monitoring data in 26 patients, exercise electrocardiograms in 21 patients, and invasive electrophysiologic data in 61 patients. Surface electrocardiograms showed normal sinus rhythm in 52%, sinus node dysfunction in 27%, and atrioventricular block in 16%. Holter monitoring was obtained in an unselected subgroup of 26 patients who had a mean age of 12 years and a mean interval from operation of 9 years. Sinus node dysfunction was found in 58%, atrioventricular block in 27% ventricular ectopy in 50%, supraventricular ectopy in 27%, and no abnormalities in only 8%. Intracardiac electrophysiologic evaluation showed a high frequency of abnormal sinus node recovery times and suboptimal response of the atrioventricular-conduction system to rapid atrial pacing. When all modalities used in this study were considered, sinus node dysfunction occurred in 47%, ectopy in 34% and atrioventricular block in 23%. Although only 30% of patients had no evidence of arrhythmia, symptoms of rhythm or conduction disturbances were rare.

Sequelae of atriotomy and ventriculotomy on the endocardium, conduction system and coronary arteries.

The endocardium was analyzed in all four chambers of 99 hearts with various types of congenital heart defects in which surgical repair was performed more than 6 weeks before death. The findings were compared with those of normal hearts in similar age groups. In some cases the endocardium was microscopically examined. This study revealed that in many cases all four chambers had fibroelastosis of the endocardium (diffuse regardless of the type of surgery done previously). These data suggest that diffuse fibroelastosis can occur as a result of surgical intervention and may be related to blocked lymphatic drainage. Sudden death in some patients long after surgery for congenital heart disease and the failure of the chambers to regress to normal size in some cases after total surgical repair may be related to fibroelastosis of the chambers. The sinoatrial node may be injured in atriotomy and in the performance of the Mustard procedure. Ventriculotomy may injure the right bundle branch. Ventriculotomy may also injure the coronary supply to the right ventricle or rarely the anterior descending coronary artery.

Pathology of the sinus node in d-transposition following the Mustard operation.

In a pathological study of 32 necropsy specimens from patients with d-transposition who had undergone the Mustard operation, lesions were commonly present in the sinus nodal artery, the sinus node, and the paranodal tissues. These had resulted from surgical injury during placement of the atrial baffle and/or closure of the atriotomy incision. Our findings confirm the pathological findings of others. The pathological observations correlate well with reported electrophysiological studies that show frequent occurrence of postoperative supraventricular arrhythmias due to sinus nodal dysfunction. Twenty-six of the patients died in the early postoperative period, and the sinus nodal artery had been compressed by sutures in 46 percent of these cases. The sinus node either showed acute necrosis or compression by sutures in 77 percent of cases, and the paranodal areas were involved by acute hemorrhage and/or necrosis in 100 percent of cases. Six patients died in the late postoperative period. The sinus nodal artery was replaced by fibrous tissue in three and was compressed or thrombosed in two additional instances. The sinus node was extensively fibrosed in each of the six cases. In every instance, the paranodal areas were involved by fibrosis and disruption by sutures.