Pseudo-polymorphic Ventricular Tachycardia in a 12-lead Holter Recording

Here, we present an image of pseudo-polymorphic ventricular tachycardia recording on a 12-lead surface ECG Holter. Although at first glance the appearance of the recording resembled polymorphic ventricular electrocardiographic findings. tachycardia , careful investigation revealed a normal A 58 year old asymptomatic hypertensive patient was referred to our center for further investigation (performance of an electrophysiological study) due to a polymorphic ventricular tachycardia (VT) seen on the 12-lead surface ECG Holter strip recording (Figure below).

 

-The patient was a professional truck driver and the 24-hour ECG Holter recording had been performed for insurance reasons .
1- After a careful revision of the tracing, it was noted that the last QRS complexes in both the limb and the precordial leads (blue arrows) were narrow and exhibited near normal morphology.
2- Similar complexes also appeared during the ongoing tachycardia between the wide QRS complexes (red arrows).
3-The underlying rhythm was of sinus origin (circle), as assumed by a P wave preceding the last QRS complex in the majority of the leads. This was confirmed by the appearance of regular QRS complexes with normal cycle length among the "polymorphic tachycardia" waveforms in the precordial lead recordings.
4-The diagnosis of polymorphic VT was based on the wide QRS complexes, which turned out to be electrocardiographic artifacts. Indeed, an accurate analysis of the trace revealed an underlying normal heart rhythm.
5-The mechanism behind this artifact lies in the "tapping" of the external electrodes depending on the patient's activities during the recording. Common sources of artifacts in analog recorders include electrode displacement, cable rupture, myopotentials, body movement or repeated regular tapping on the chest wall during chest physiotherapy or breathing exercises .
Based on the aforementioned analysis of the Holter tracing, we decided not to conduct any further diagnostic testing.
Presently, two years after this incident, the patient is still asymptomatic and in good physical condition.
6-Electrocardiographic artifacts can closely simulate VT and can sometimes be misdiagnosed as such, resulting in unnecessary and potentially dangerous medical treatment or interventions .
7-In order to prevent artifacts during a Holter recording, the integrity of the electrodes must be evaluated and the patient be advised to avoid intense body movements or exercise.
In addition, physicians must be experienced and able to recognize such artifacts to avoid an erroneous diagnosis.
Reference:
George Nikitas MD, Christos Maniotis MD, George Manolis MD, and Athanasios G. Manolis MD
Hellenic Red Cross Hospital of Athens, Greece

Pulmonary arterial hypertension as a medium-term risk of death in patients ith heart failure

A decade ago, the diagnosis of pulmonary arterial hypertension (PAH) heralded a uniformly poor prognosis. Progress has come in recent years via the development of carefully targeted therapies.

Heart failure (HF) is one of the most common causes of PH, - See more at: http://www.acc.org/latest-in-cardiology/articles/2015/04/14/15/21/left-heart-disease-check-for-pulmonary-hypertension-practical-approaches-to-the-management-of-pulmonary-hypertension#sthash.aXt4vyUX.dpuf

A growing appreciation that pulmonary hypertension (PH) in left heart disease (LHD) signals poor prognosis has led to a flurry of investigational activity.
Heart failure (HF) is one of the most common causes of PH.
There was a strong, positive, graded association between PA (Pulmonary Artery)  systolic pressure and subsequent mortality that was independent of age, sex, comorbidities, EF, and diastolic function. The investigators found that PA systolic pressure strongly predicted medium-term risk of death in patients with HF( Heart failure)  and improved prediction of death and CV death over traditional prognostic factors. Importantly, PH( pulmonary hypertension ) appeared to be not only a marker of worse HF, but also to have direct deleterious effects.

PH   in HF has been postulated to result from the combination of the passive effect of elevated left ventricular end-diastolic pressure backward on the pulmonary venous circulation and an active vasoreactive process of vasoconstriction and PA remodeling. Pathology studies have shown remodeling changes in the elastic fibers of the pulmonary arterial wall, intimal fibrosis, and medial hypertrophy of pulmonary muscular arteries, with changes that are similar to or greater than those seen in idiopathic PAH.

Although PAH and PH secondary to LHD share a final common hemodynamic and prognostic outcome, translational investigations have suggested fundamental differences in the cellular basis and in outcomes related to pharmacological modulation of neurohormonal pathways in these distinct states. For example, the presence of the angiotensin-converting enzyme DD genotype is associated with adverse survival in LV failure, whereas in PAH, there are signals supporting a compensatory role in preserving right ventricular (RV) function. Similarly, beta-adrenergic neuroeffector pathways demonstrate distinct differences between right-side HF due to PAH or PH secondary to LHD.

 
Despite evidence for the expression of endothelin-1 excess in both PAH and LHD states, the outcome of targeting the aberration through endothelin antagonists is quite dissimilar, with a marked evidence of benefit in PAH but notable worsening in the context of LHD. Conversely, therapeutic modulation of the nitric oxide pathway with the use of phosphodiesterase-5 inhibitors may be equally beneficial between the two distinct syndromes of PAH and PH due to LHD.

Reference:

LeftHeart Disease? Check for Pulmonary Hypertension: Practical Approaches to theManagement of Pulmonary Hypertension

PH in HF has been postulated to result from the combination of the passive effect of elevated left ventricular end-diastolic pressure backward on the pulmonary venous circulation and an active vasoreactive process of vasoconstriction and PA remodeling. Pathology studies have shown remodeling changes in the elastic fibers of the pulmonary arterial wall, intimal fibrosis, and medial hypertrophy of pulmonary muscular arteries, with changes that are similar to or greater than those seen in idiopathic PAH. - See more at: http://www.acc.org/latest-in-cardiology/articles/2015/04/14/15/21/left-heart-disease-check-for-pulmonary-hypertension-practical-approaches-to-the-management-of-pulmonary-hypertension#sthash.aXt4vyUX.dpuf

There was a strong, positive, graded association between PA systolic pressure and subsequent mortality that was independent of age, sex, comorbidities, EF, and diastolic function. The investigators found that PA systolic pressure strongly predicted medium-term risk of death in patients with HF and improved prediction of death and CV death over traditional prognostic factors. Importantly, PH appeared to be not only a marker of worse HF, but also to have direct deleterious effects. - See more at: http://www.acc.org/latest-in-cardiology/articles/2015/04/14/15/21/left-heart-disease-check-for-pulmonary-hypertension-practical-approaches-to-the-management-of-pulmonary-hypertension#sthash.aXt4vyUX.dpuf