Intrinsic SND is due to either abnormalities of the sinus node or contiguous atrial tissue. The etiology is usually degeneration with scarring of the sinus node and perinodal atrial tissue. SND may also arise from other conditions associated with degeneration or destruction of these structures, including myocardial infarction, restrictive or congestive cardiomyopathies, and some cardiac surgeries most notably for correction of congenital heart disease.
Extrinsic SND results from other causes thyroid disorders, drugs or drug interactions, disorders of or affecting the autonomic nervous system, or extreme body temperatures. The diagnosis is made electrocardiographically. SND may manifest with atrial bradyarrhythmias, tachyarrhythmias, or a combination of the two. It is commonly accepted that ambulatory sinus pauses of greater than 3 seconds in duration are rare and may indicate SND. Sinus pauses may be due to either sinus arrest or sinus exit block.
Other rhythms associated with or indicative of SND are severe sinus bradycardia, paroxysmal atrial tachyarrhythmias classically with associated bradyarrhythmias with or without posttachyarrhythmia conversion pauses, the so-called tach-brady syndrome , and chronic atrial fibrillation with slow ventricular rates in the absence of AV nodal blocking pharmacologic therapy.
Chronotropic incompetence is another manifestation of SND. It is the inability to increase heart rate with exercise. There exist varying quantitative criteria for defining chronotropic incompetence. One is the inability to achieve a maximal exercise heart rate of bpm. SND may first manifest after initiation of antiarrhythmic drugs. If the first manifestation of the SND is with pharmacologic therapy that may be discontinued or there exists an alternative drug, cessation of the drug and observation with prolonged monitoring may be appropriate to differentiate between intrinsic and extrinsic SND.
Usually there is underlying intrinsic physiologic substrate for SND if pharmacologic therapy causes SND, though it might not be clinically apparent or significant. Symptoms may or may not be present. The absence or presence of symptoms is not necessary for the diagnosis of SND, though it is the determinant of therapeutic recommendations.
Extrinsic causes are addressed with assessment of medications, blood tests for thyroid abnormalities , and evaluation for associated autonomic dysfunction, if suspected. The typical patient with SND presents with arrhythmias detected via electrocardiogram ECG , ambulatory monitoring hour recording, prolonged electrocardiographic event monitoring, or outpatient telemetry recordings see diagnostic tests below.
The recordings may have been prompted as a part of the routine exam ECG , or in the case of monitoring, prompted by findings found on a lead ECG or by symptoms. Symptoms are diverse, corresponding to a broad range of electrocardiographic manifestations. They may include palpitations due to PACs, paroxysmal atrial tachycardias, or atrial fibrillation , fatigue from bradycardia or chronotropic incompetence , light-headedness, or syncope from pauses. More unusual symptoms may include cognitive abnormalities, periodic polyuria related to atrial distention with release of atrial natriuretic peptide experienced with or immediately after paroxysmal atrial tachycardia or atrial fibrillation , and thromboembolic phenomena from bradycardia-induced hypoperfusion of a stenotic vessel or embolic related to atrial fibrillation.
As many times symptoms are present without electrocardiographic findings and nonspecific electrocardiographic findings present without symptoms, the correlation of electrocardiographic abnormalities with symptoms is paramount in establishing a causal relationship to best determine the most appropriate therapeutic approach. The prevalence of SND is not known because so many patients are asymptomatic.
In addition, the criteria for defining a heart rate or pause as abnormally slow are more dependent on the association of symptoms than an arbitrary number.
SND is usually diagnosed in the seventh and eighth decades of life, with an average age of 65 in a few studies. There are rare familial cases of SND that may manifest in younger patients, some of which may be associated with long Q—T syndrome. The differential diagnosis of SND includes chronically high vagal tone [usually manifest as chronic sinus bradycardia, which may be marked, or sinus pauses during sleep, which may be accompanied by varying degrees of second-degree atrioventricular AV block with or without AV dissociation ].
These patients are asymptomatic, are often young, and are usually in excellent physical condition and athletic. Thyroid disease must be ruled out because it requires specific treatment, which generally results in resolution of the arrhythmia problem. Physical examination is rarely helpful in establishing a diagnosis. A resting bradycardia on examination is usually not associated with symptoms in patients with SND. Correlation of diagnostic electrocardiographic abnormalities is what is necessary to best guide management decisions. The resting electrocardiogram is usually unrevealing or demonstrates nondiagnostic abnormalities without symptoms.
The next step should be to obtain ambulatory monitoring. This may be a hour test which has a very low yield but may be mandated by the insurer prior to longer term monitoring. If the hour monitoring is unrevealing, or if symptoms occur on a less frequent than daily basis, then a prolonged monitor with an event recorder or outpatient telemetry is warranted. There is growing evidence that premature atrial complexes PAC may be associated with the development of AF, and therefore with an increased risk of stroke. They identified individuals with frequent episodes of paroxysmal AF and mapped which rhythms commonly preceded the onset of AF.
The trigger was often a PAC originating from a pulmonary vein, and radiofrequency ablation of this area of ectopic activity led to decreased recurrence in arrhythmic activity. Wallmann et al.
Evaluation and Treatment of Sick Sinus Syndrome - The Cardiology Advisor
Patients were then grouped according to their total burden of PAC over the 7-day period. The Copenhagen Holter study 5 investigated AF prevalence and its effect on morbidity and mortality and was one of the largest studies of its kind in healthy individuals. Investigators contacted all men aged 55 years, and all men and women aged 65, 70, and 75 years in two different areas of the city.
Individuals with previous cardiovascular ill health were excluded, leaving participants who went on to complete hour ambulatory ECG monitoring. In , Binici et al. Using a more clinically applicable approach, Larsen et al. The intervention arm of the EMBRACE trial 9 was used to investigate the prevalence of subclinical AF in patients who had suffered either a transient ischaemic attack or cryptogenic stroke. Recruits underwent hour ambulatory ECG monitoring and, if AF was not detected on initial monitoring, they were then assigned to day external loop recording.
Higher burdens of premature ventricular complexes PVC post myocardial infarction are associated with a poorer prognosis. In patients with underlying structural heart disease, PVC can trigger ventricular arrhythmia, 12 but in individuals with structurally normal hearts they are often considered a benign process that does not require treatment or intervention. Patients with resting ventricular ectopy had a significantly increased risk of all-cause and cardiovascular mortality. They also categorised patients by heart rate and showed mortality to increase with heart rate and to double in the presence of PVC.
The presence of PVC has been linked with incidental heart failure. Further work by Agarwal et al. A high frequency of PVC may result in left ventricular systolic dysfunction. In , Baman et al. Penela et al. Patients with high ectopic burdens who met the criteria for ICD implantation had the ICD withheld and instead underwent ventricular ectopic ablation.
They were followed up at 6 and 12 months. The Brugada syndrome: facts and controversies. Herz May;32 3 Clinical aspects and prognosis of Brugada syndrome in children. Circulation April 17; 15 Electrical storm in Brugada syndrome successfully treated using isoprenaline. Europace March;6 2 Electrical storms in Brugada syndrome: review of pharmacologic and ablative therapeutic options.
Indian Pacing Electrophysiol J ;5 1 Fever and Brugada syndrome. Pacing Clin Electrophysiol November;25 11 Rev Esp Cardiol May;53 5 You may send an e-mail here should you wish to receive pubmed links to articles listed in reference. Our mission: To reduce the burden of cardiovascular disease. All rights reserved. Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more. Sign in to My ESC.
ESC sub specialties communities. Read your latest personalised notifications Sign in No account yet? Don't miss out Read your latest personalised notifications Ok, got it. Loading quicklinks Josep Brugada. It should be stressed that type 1 is the only ECG diagnostic pattern of BS while types 2 and 3 should only be considered suggestive of the disease4, 5. Step 3 : excluding the idiopathic Brugada ECG pattern-prognosis Once we have observed a type 1 ECG in more than 1 precordial leads, and exclude other conditions that may account for it, we should search for clinical data that support the diagnosis of BS.
ECG type 1 in family members Arrhythmia-related symptoms: Syncope. Nocturnal agonal respiration. Documented ventricular arrhythmias: Polymorphic ventricular tachycardia PVT. Ventricular fibrillation VF. Spontaneous ECG type 1 is not an independent predictor of ventricular arrhythmias in multivariate analysis of the largest registries on the subject26, 27; but it still identified a subgroup of patients with a higher risk of future arrhythmic events when combined with history of syncope and inducibility during electrophysiological EP study.
Males show a tendency to develop more arrhythmic events than women and have a worse prognosis during follow-up2. The value of inducibility of sustained ventricular arrhythmias during EP study as a risk predictor tool in BS is still the most controversial topic.
The results of the largest BS registry indicates that inducibility during EP study is an independent predictor for cardiac events hazard ratio: 8. There are several proposed reasons that may account for this and other differences among the registries: different inclusion criteria, different stimulation protocols, different statistical analysis methods, etc. Prospective studies to elucidate the role of EP study in the risk stratification of these patients are currently being performed. Step 6 : Recommendations BS patients should be recommended to avoid all drugs that may induce a type 1 class ECG table 3.
As fever may elicit the diagnostic ECG pattern, and has also been recognized as a trigger of ventricular arrhythmias in BS42, 43, patients should be encouraged to treat it aggressively. Patients must contact their cardiologist immediately in case of presenting syncope, seizures or nocturnal agonal respiration. Family screening of BS is strongly recommended in first-degree relatives BS is an inherited disease, transmitted in an autosomal-dominant way. All patients must have regular follow-up, in order to identify the development of symptoms.
Genetic testing, when available, is recommended 5 to support clinical diagnosis, early detection of other affected family members and for researching purposes. But diagnosis should not be based on it, since it still have a low diagnostic yield. Sodium channel blockers: Class IC drugs Flecainide, propafenone, pilsicainide. Class IA drugs Ajmaline, procainamide, dysopiramide, cibenzoline 2. III-Antianginal drugs: 1. Calcium channel blockers: Nifedipine, diltiazem 2.