Wednesday, May 18, 2016

64-Year-Old Woman with a History of Aortic Valve Disease and Primarily Aortic Regurgitation

 A 64-year-old woman with a history of aortic valve disease, primarily aortic regurgitation who presents to the emergency room with the acute onset of palpitations associated with shortness of breath. What does the ECG show?


Response: Regarding the 64-year-old woman with a history of aortic valve disease, primarily aortic regurgitation.

Diagnosis: atrial tachycardia terminating to sinus tachycardia with premature atrial complex, low voltage precordial leads

The initial portion of the ECG shows a regular rhythm at a rate of 180 bpm. There is an abrupt slowing to a rate of 100 bpm. The QRS complex has a normal duration (0.08 sec) and normal morphology. The axis is normal between -0° and +90° (positive QRS complex in lead I and aVF). There is low voltage in the precordial leads, defined as an amplitude <10 mm in each lead. The QT/QTc intervals are normal (280/415 msec). Although P waves are not obvious during the first portion of the ECG, there are prominent positive waveforms noted within the ST segments, particularly in leads I, II, and aVF (v). These are P waves and hence this is a short RP (0.14 sec) (└┘) and long PR (0.24 sec) (┌┐) tachycardia. Etiologies for a short RP tachycardia included:
1. sinus tachycardia
2. atrial tachycardia
3. atrial flutter
4. ectopic junctional tachycardia
5. atrioventricular nodal reentrant tachycardia
6. atrioventricular reentrant tachycardia
    After the tachycardia terminates, there is a regular rhythm at a rate of 100 bpm. There is a P wave before each QRS complex with a constant PR interval (0.14 sec). The P waves are positive in leads I and V5-V6; this is likely a normal sinus rhythm. There is one premature QRS complex (*) which is preceded by a P wave (↓) with a different morphology compared to the sinus P waves; this is a premature atrial complex. As the PR interval of the sinus rhythm is shorter than the PR interval during the tachycardia, the tachycardia is not sinus tachycardia in which the PR interval should be the same or shorter when compared to the normal sinus rhythm. Important for the diagnosis is the way the tachycardia terminates. Noted is that it terminates without atrial activity (↑) which is the mode of termination of atrial arrhythmias. Given the rate and the fact that the atrial waveforms are positive in leads II and aVF, this is an atrial tachycardia, terminating to sinus tachycardia.


Tuesday, May 17, 2016

Invasive Assessment of Coronary Physiology

CME COURSE

Invasive Assessment of Coronary Physiology Predicts Late Mortality After Heart Transplantation
 

Abstract
Background
—The aim of this study is to determine the prognostic value of invasively assessing coronary physiology early after heart transplantation.
Methods and Results—Seventy-four cardiac transplant recipients had fractional flow reserve, coronary flow reserve, index of microcirculatory resistance (IMR), and intravascular ultrasound performed down the left anterior descending coronary artery soon after (baseline) and 1 year after heart transplantation. The primary end point was the cumulative survival free of death or retransplantation at a mean follow-up of 4.5±3.5 years. The cumulative event-free survival was significantly lower in patients with a fractional flow reserve <0.90 at baseline (42% versus 79%; P=0.01) or an IMR ≥20 measured 1 year after heart transplantation (39% versus 69%; P=0.03). Patients in whom IMR decreased or did not change from baseline to 1 year had higher event-free survival compared with patients with an increase in IMR (66% versus 36%; P=0.03). Fractional flow reserve <0.90 at baseline (hazard ratio, 0.13; 95% confidence interval, 0.02–0.81; P=0.03), IMR ≥20 at 1 year (hazard ratio, 3.93; 95% confidence interval, 1.08–14.27; P=0.04), and rejection during the first year (hazard ratio, 6.00; 95% confidence interval, 1.56–23.09; P=0.009) were independent predictors of death/retransplantation, whereas intravascular ultrasound parameters were not.
Conclusions—Invasive measures of coronary physiology (fractional flow reserve and IMR) determined early after heart transplantation are significant predictors of late death or retransplantation.

Wednesday, May 11, 2016

67-Year-Old Woman with Hypertension and Mitral Regurgitation

A 67-year-old woman with known hypertension and mild mitral regurgitation who presents to the emergency room with the acute onset of palpitations. Her pulse is noted to be irregular.






Diagnosis: atrial fibrillation, Ashman’s phenomenon

The rhythm is irregularly irregular with an average rate of 102 bpm. All the QRS complexes (except for the 11th complex [*]) have the same normal duration (0.08 sec) and normal morphology. Their axis is normal between 0° and +90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (320/420 msec). There are only three supraventricular rhythms that are irregularly irregular. These are:
1.sinus arrhythmia in which there is one P wave morphology and PR interval
2.multifocal atrial rhythm or wandering atrial pacemaker (rate <100 bpm) or multifocal atrial tachycardia (rate >100 bpm) in which there are ≥ 3 different P wave morphologies (and often different PR intervals) without any one P wave morphology being dominant
3. atrial fibrillation in which there are no organized P wave
In this case, there are no organized P waves seen, but there are prominent low amplitude undulations of the baseline (^) which are irregular in amplitude, interval, and morphology. Therefore the rhythm is atrial fibrillation. Complex 11 has a different morphology. It is wider (0.12 sec) and has a right bundle branch block morphology with an RSR’ in lead V! (→). This is not a rate related right bundle branch block as there are other RR intervals that are as short or shorter than that preceding this QRS complex. However, it can be seen that this QRS complex is preceded by a long (↔) short (└┘) RR interval. Therefore this aberrated complex is the result of the Ashman’s phenomenon. This is the result of rate related changes in His-Purkinje refractoriness and not the result of conduction abnormalities. Whenever heart rate is slower, His-Purkinje refractoriness is longer and when heart rate is faster, His-Purkinje refractoriness shortens.  When there is an abrupt change in rate, i.e. slower or long RR interval to faster or short RR interval, His-Purkinje refractoriness may not adapt immediately and hence one  or several QRS complexes will be conducted with aberration. Most often there is a right bundle branch block.