The coronary-to-pulmonary artery fistulas are usually discovered incidentally during routine cardiac catheterization after the development of atherosclerotic coronary artery disease.We report the incidental finding of two cases of coronary-to-pulmonary artery fistulas who presented with acute coronary syndrome.
A 90-year-old woman with hypertension and a history of a dual-chamber, rate-modulated (DDDR) pacemaker implantation 9 years previously presented to the hospital with complaints of syncope, moderate shortness of breath, and a headache. She denied any other symptoms. Her vital signs were as follows: blood pressure, 110/80 mmHg; pulse, 35 beats/min (bpm); and respiratory rate, 18 breaths/min. One month before presentation, she had undergone pacemaker replacement due to battery depletion at another hospital. The electrocardiogram (ECG) on admission is shown in Fig. 1. Pacemaker interrogation showed the following parameters: programmed mode, DDDR with a base rate of 60 bpm; atrial impedance, 410 Ω; ventricular impedance, 540 Ω; atrial sensing threshold, 0.5 mV; ventricular sensing threshold, 2.0 mV; and battery voltage, 2.6 V. The paced and sensed atrioventricular intervals (AVIs) were 150 and 120 ms, respectively. The pacemaker was switched to AAI mode, and the corresponding ECG is shown in Fig. 2. Twelve-lead electrocardiogram on admission. Twelve-lead electrocardiogram in AAI mode. Atrial lead dislodgement The atrial and ventricular leads are switched Ventricular noncapture Crosstalk Pacemaker undersensing The correct answer is B. In patients with a previously implanted device, pacemaker malfunction is a very rare cause of syncope. On initial evaluation, the pacing spike in our patient only appeared after QRS complexes on the ECG at admission, which is suggestive of undersensing; however, pacemaker interrogation showed normal sensing thresholds and impedances. Undersensing can be due to various factors such as low sensitivity settings, lead insulation defects, event falls within a refractory period (i.e., functional undersensing), too slow of a slew rate, and malfunction of the pacemaker circuitry [1]. The most common causes of noncapture include lead displacement, an insulation defect, wire fracture, electrolyte disturbance, and exit block (a high capture threshold). Atrial noncapture can be detected by the absence of a P-wave and the sudden appearance of a wide complex QRS, whereas during ventricular noncapture, paced output occurs without depolarization of the ventricle, which results in an asystolic pause [1]. Crosstalk is characterized by the inhibition of ventricular output due to the ventricular channel sensing of an atrial pulse. It is seen on the ECG strip as paced atrial P-waves without ventricular output. Crosstalk is rarely seen with current dual-chamber pacemakers because of the ventricular blanking period [2]. In the present case, the pacing spikes were evidently synchronized with the QRS complexes, with a 150-ms interval between two spikes. This pattern only occurs when the leads are switched (Fig. 1). Moreover, the period without pacing only contains F-waves, which strongly suggests that atrial events inhibit output from the ventricular channel of the pacemaker. When the atrial and ventricular leads are switched, the designated sensed event in the ventricular channel is actually an atrial event. Ventricular pacing through the atrial lead can cause atrial fibrillation, hypotension, and clinical heart failure due to 1:1 retrograde atrial activation. Atrial lead dislodgement to the ventricle should be briefly considered; however, since ventricular pacing in such a situation would be inhibited or within the atrioventricular safety window, this diagnosis is incorrect. The diagnosis of switched leads in a permanent pacemaker is usually made within a few hours or days after implantation, but this complication is rarely overlooked in the long-term, as in the present case [2]-[4]. In conclusion, the possibility that the atrial and ventricular leads of a pacemaker generator are switched should be considered, especially in patients who present early after battery replacement. None.
The most important sequel of acute rheumatic fever is mitral stenosis in long-term. The aim of the study is to determine left ventricular (LV) functions by tissue Doppler imaging (TDI) and strain/strain rate echocardiography (SE/SRE) in mitral stenosis patients who had no clinical signs of heart failure.Our study was designed as cross-sectional study. The study population consisted of 32 patients with isolated mitral stenosis and mitral valve area = 2.0 cm(2) (Group 1) and 25 healthy control subjects (Group 2). In addition to standard echocardiographic methods, TDI and SE/SRE were performed to assess LV functions in all participants. Student's t-test was used to compare continuous variables. Fisher- exact test was used to compare categorical variables.Systolic myocardial velocity (Sm) were significantly lower in Group 1 than in Group 2 (6.0+/-1.4 cm/sec vs 7.9+/-1.8 cm/sec, p=0.001) also, early diastolic myocardial velocity (Em) were significantly lower in Group 1 than in Group 2 (4.4+/-1.5 cm/sec vs 10.8+/-2.1 cm/sec, p=0.001). But there was no significant difference in late diastolic myocardial velocity (Am) between two groups. Peak systolic strain and strain rate of septal wall in Group 1 were significantly lower than Group 2 (p=0.001 for both). Besides, peak systolic strain and strain rate of lateral wall in Group 1 were significantly lower than in Group 2 (p=0.001 for both).Although, global ejection fraction was normal and there were no symptoms of heart failure clinically in the patients with mitral stenosis, LV dysfunction demonstrated that using by echocardiography. TDI and strain/strain rate imaging to be new echocardiographic methods may be used reliably for detection LV function in early stage of mitral stenosis.
We evaluated regional left atrial (LA) myocardial deformations by strain (S) and strain rate (SR) imaging during LA pump, reservoir, and conduit phases in patients with chronic rheumatic mitral regurgitation (MR).This cross-sectional observational study included 42 patients with moderate-to-severe MR who had normal left ventricular (LV) function, and 36 healthy control subjects. Conventional echocardiographic data were used to calculate LV and LA dimensions, volumes and functional indices (LA ejection fraction, LA active and passive emptying fraction). Longitudinal S/SR indices of the mid and superior segments of LA walls were measured during the three LA phases. Student t-test, Mann-Whitney U test, Chi-square test and Bland-Altman analysis were used for statistical analysis.LV systolic functions were similar in the patient and control groups. LV diameters, LA diameters and LA volumes were greater in the patient group compared with the control group (p<0.05, p<0.001, and p<0.001). LA ejection fraction and LA active emptying fraction values were lower in the patient group than in the control group (56 ± 7 vs. 63 ± 5%, 33 ± 9 vs. 40 ± 4%, p<0.05 for both). During the three LA phases, longitudinal S/SR values were significantly lower in all the segments in the patient group compared with the control group (p<0.001 for S, p<0.001 and p<0.05 for SR).Regional LA longitudinal myocardial deformations are observed to be impaired during all the mechanical phases in patients with moderate-to-severe MR. Volume overload, remodeling and rheumatic effects may be responsible for the LA myocardial dysfunction in these patients.