Cardiac Rhythm Device Threshold Testing Via Pulse Oxymetry.

Threshold testing of cardiac rhythm devices is essential to monitoring the proper functioning of such devices (1). However, the currently method of applying multiple ECG leads to the patient is burdensome and time consuming (2). We are presenting a completely new way to perform cardiac rhythm device threshold testing using pulse oximetry. Twenty patients, with varying cardiac rhythm devices and pacing modes, were enrolled and had their atrial and ventricular thresholds tested. A comparison was made between simultaneous threshold determinations via the standard EGM based method and the new pulse oximetry based method. 75% of the ventricular threshold tested and 58% of the atrial thresholds tested were the same with the two testing methods. The remainder of the tests (25% of ventricular threshold and 42% of the atrial threshold tests) varied by +0.25 V. This study shows that pulse oximetry based testing is an accurate, reliable, and easy way to perform cardiac rhythm device threshold testing and may complement traditional methods to perform such tests in the future.

Path length entropy analysis of diastolic heart sounds.

Early detection of coronary artery disease (CAD) using the acoustic approach, a noninvasive and cost-effective method, would greatly improve the outcome of CAD patients. To detect CAD, we analyze diastolic sounds for possible CAD murmurs. We observed diastolic sounds to exhibit 1/f structure and developed a new method, path length entropy (PLE) and a scaled version (SPLE), to characterize this structure to improve CAD detection. We compare SPLE results to Hurst exponent, Sample entropy and Multiscale entropy for distinguishing between normal and CAD patients. SPLE achieved a sensitivity-specificity of 80%-81%, the best of the tested methods. However, PLE and SPLE are not sufficient to prove nonlinearity, and evaluation using surrogate data suggests that our cardiovascular sound recordings do not contain significant nonlinear properties.

Noise detection in heart sound recordings.

Coronary artery disease (CAD) is the leading cause of death in the United States. Although progression of CAD can be controlled using drugs and diet, it is usually detected in advanced stages when invasive treatment is required. Current methods to detect CAD are invasive and/or costly, hence not suitable as a regular screening tool to detect CAD in early stages. Currently, we are developing a noninvasive and cost-effective system to detect CAD using the acoustic approach. This method identifies sounds generated by turbulent flow through partially narrowed coronary arteries to detect CAD. The limiting factor of this method is sensitivity to noises commonly encountered in the clinical setting. Because the CAD sounds are faint, these noises can easily obscure the CAD sounds and make detection impossible. In this paper, we propose a method to detect and eliminate noise encountered in the clinical setting using a reference channel. We show that our method is effective in detecting noise, which is essential to the success of the acoustic approach.

Unusual pauses in sinus rhythm and intermittent 2 to 1 AV block in a patient with concealed his extra systoles--a rare cause of bradycardia.

A 56 year old male with a past medical history of hypertension and dyslipidemia presented with recurrent dizziness. Routine EKG was performed, which suggested frequent junctional extra systoles with compensatory pauses. During telemetry periods of 2:1 block with effective ventricular rate of 34 bpm was observed. His bundle study suggested frequent His extra systoles causing functional AV block. Treatment with anti-arrhythmic medication, paradoxically improved AV block and symptoms in our patient.

Rate smoothing induced ventricular arrhythmia and syncope: a new device-induced proarrhythmia.

A 74-year-old male presented to our emergency room with history of sudden onset palpitations associated with syncope. He had a single-chamber implantable cardioverter defibrillator implanted for secondary prevention of sudden cardiac death due to ischaemic cardiomyopathy. Interrogation of the device revealed episodes of non-sustained ventricular tachycardia (NSVT) at 220 ms. Post-tachycardia, another episode of NSVT with longer duration, was induced by rate smoothing pacing algorithm following premature ventricular beats. We describe this unique form of device-related proarrhythmia causing syncope.

Atrial flutter with spontaneous 1:1 atrioventricular conduction in adults: an uncommon but frequently missed cause for syncope/presyncope.

AIMS: To compare patients with atrial flutter (AFl) and 1:1 atrioventricular conduction (AVC) with patients with AFl and higher AVC. METHODS: The characteristics of 19 patients with AFl and 1:1 AVC (group A) were compared with those of 116 consecutive patients with AFl and 2:1 AVC or higher degree AV block (group B). RESULTS: Age, gender, and left ventricular function were similar in the two groups. In group A versus group B, more patients had no structural heart disease (42% vs 17%, P < 0.05) and syncope/presyncope (90% vs 12%, P < 0.05). The AFl cycle length (CL) in group A was longer than in group B (265 +/- 24 ms vs 241 +/- 26 ms, P < 0.01). The transition from AFl with 1:1 to 2:1 AVC or vice versa was associated with small but definite changes in AFl CL, which showed larger variations in response to sympathetic stimulation. In group A patients who were studied off drugs, the atrial-His interval was not different from group B, but maximal atrial pacing rate with 1:1 AVC was faster. In group A, five patients were misdiagnosed as ventricular tachyarrhythmias, and three with a defibrillator received inappropriate shocks. Four patients had ablation of AVC and six had ablation of AFl circuit. CONCLUSIONS: The main difference between groups A and B may be an inherent capacity of the AV node for faster conduction, especially in response to increased sympathetic tone. The latter affects not only AVC but also the AFl CL. One should be aware of the different presentations of AFl with 1:1 AVC to avoid misdiagnosis/mismanagement and to consider the diagnosis in patients with narrow or wide QRS tachycardia and rates above 220/min.

Prolonged transient atrial electrical silence following termination of chronic atrial tachyarrhythmias.

INTRODUCTION: Atrial standstill is a rare heterogeneous arrhythmia characterized by electrical and mechanical standstill and electrical inexcitability. A long-lasting progressive form is seen with cardiac and neuromuscular diseases, and a familial or idiopathic form may have a genetic basis. A transient form was described secondary to drug intoxication, electrolyte imbalance, cardiac inflammation, and ischemia. METHODS: We investigated three patients with long-standing atrial tachyarrhythmia (AT) (atrial flutter in two, and focal atrial tachycardia in one). All patients underwent a complete electrophysiological study with mapping of right and left atrial activity and radiofrequency ablation (RF Abl) of AT. RESULTS: Following RF Abl of AT, all three patients manifested transient atrial electrical silence in the absence of known reversible causes. Atrial electrical silence was observed when, following AT termination, an escape atrioventricular (AV) junctional rhythm (in two patients) and an escape VVI pacemaker rhythm (in one patient) showed transient ventriculo-atrial (VA) conduction block (up to 30 seconds). A dominant sinus rhythm was observed to return 30 minutes, 90 minutes, and 12 hours, respectively, in the three patients. Two patients received a dual chamber pacemaker and a decision was made not to upgrade the patient with VVI pacemaker. DISCUSSION AND CONCLUSIONS: The present report expands the spectrum of the syndrome of atrial standstill and raises interesting questions regarding possible electrophysiologic mechanism(s) of prolonged post overdrive atrial standstill. The report suggests that chronic overdrive of sinus and subsidiary atrial pacemakers may result in calcium overloading of cardiac cells, which is known to cause suppression of pacemaker activity as well as increased intracellular resistance. These mechanisms can possibly result in either prolonged suppression of sinus and atrial pacemaker activity and/or pacemaker exit block.

Left bundle branch block in type 2 diabetes mellitus: a sign of advanced cardiovascular involvement.

OBJECTIVE: To evaluate left bundle branch block (LBBB) as an indicator of advanced cardiovascular involvement in diabetic (DM) patients by examining left ventricular systolic function and proteinurea. METHODS: Data of 26 diabetic patients with left bundle branch block (DM with LBBB) were compared with data of 31 diabetic patients without left bundle branch block (DM without LBBB) and 18 nondiabetic patients with left bundle branch block (non-DM with LBBB). The inclusion criteria were age >45 years, and diabetes mellitus type 2 of >5 years. RESULTS: Mean ages of patients in DM with LBBB, DM without LBBB, and non-DM with LBBB groups were 67 +/- 8, 68 +/- 10, and 65 +/- 10 years, respectively (P = NS). Females were 65%, 61%, and 61%, respectively (P = NS). Left ventricular ejection fraction in DM with LBBB was significantly lower than in DM without LBBB and non-DM with LBBB (30 +/- 10% vs 49 +/- 12% and 47 +/- 8%, P < 0.01). Left ventricular end-diastolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (188.6 +/- 16.4 mL vs 147.5 +/- 22.3 mL and 165.3 +/- 15.2 mL, P < 0.03). Similarly, left ventricular end-systolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (135.4 +/- 14.7 mL vs 83.7 +/- 9.5 mL and 96.6 +/- 18.4 mL, P < 0.02). No statistically significant difference was seen in left atrial size. Proteinurea in DM with LBBB (79.4 +/- 18.9 mg/dL) was significantly higher than in DM without LBBB (35.6 +/- 8.5 mg/dL, P < 0.05) and non-DM with LBBB (12 +/- 3.5 mg/dL, P < 0.05); however, there was no significant difference in Hb A1c levels in DM with LBBB and DM without LBBB (9.01% vs 7.81%, P = NS). CONCLUSIONS: Left bundle branch block in diabetic patients indicates advanced cardiovascular involvement manifesting with more severe left ventricular systolic dysfunction and proteinurea compared to both diabetic patients without left bundle branch block and nondiabetic patients with left bundle branch block.