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When arrhythmias complicate heart failures
Throughout the years, heart failure complicates usually with anomalies of the
cardiac rhythm. These anomalies can have an atrial, a ventricular or an atrioventricular
origin. A very high percentage of patients suffering heart failures, present various types of
rhythm anomalies.
Atrial arrhythmias are almost exclusively atrial fibrillations, and in a much minor
scale, atrial flutter. About a third of heart failure patients are in atrial fibrillation. The
appearance of this arrhythmia decreases the ventricular contractility with secondary
decline in the exercise tolerance.
If the atrial fibrillation has a very high ventricular rate, the ventricular diastolic time
diminishes as well as the left ventricular filing, resulting in a decreased cardiac output (the
amount of blood which the left ventricle pumps in a minute). This can only worsen the
heart failure patient’s condition which already presents a below average cardiac output
(Figure 2).
Figure 1 Multiple mechanisms by which atrial fibrillation affects symptoms, cardiac output
and the general outcome of the patients with heart failure. HF, heart failure; DF, diastolic
filling; CO, cardiac output; PE, pump efficiency; ER, embolic risk; AF, atrial fibrillation; HR,
heart rate.
More than this a “fibrillating” atrium loses contraction (or “atrial kick” from the
American authors) and this results in a 20%-30% decrease in the efficiency of the heart as
a pump. This results in a second factor which deteriorates the heart’s pumping function.
The most vulnerable hearts to atrial kick loss are the hypertrophic and/or the very dilated
ones. This loss of cardiac efficiency only increases the patient’s symptoms: the shortness
of breath increases, just like the fatigue, the sleepiness, the mental confusion and the
disordered breathing patterns during sleep can be accentuated. For the same exact
reason, the retention of liquids increases, as the body weight and the lower legs edema
appears.
The most frequent cause of death in patients with heart failure and atrial fibrillation
in the embolic stroke. In the atrial fibrillation, the loss of atrial contraction determines a sort
of “stagnation” of the blood into the atria. This phenomenon, together with the often
associated atrial enlargement, determine favourable conditions to the formations of blood
clots (thrombus), inside the atrium itself. The risk associated with this event, is that a clot
may detach from the inside of the atrium, and following the blood stream, exit the heart
and obstruct an artery. This phenomenon is called thromboembolism (see Figure 2) and if
this phenomenon involves a cerebral artery an embolic stroke is induced.
Figure 2 Anatomy of the heart, ascending aorta e carotid arteries. CE, cerebral embolism;
LA, left atrium; LV, left ventricle; PE, peripheral embolism.
Keeping in mind that the first arteries that are in the same direction as the blood that
leaves the heart are the carotid arteries, we can understand why embolisms are mainly
cerebral. The heart failure patient, even if with a normal cardiac rhythm, still presents an
elevated embolic risk, and the appearance of atrial fibrillation, for the reasons mentioned
above, can not but increase this risk. Due to all the above dangers, atrial fibrillation
appearances worsen the outcomes of the patients in heart failure.
The atrial fibrillation’s incidence increases dramatically with the gravity of the heart
failure (the NYHA class): the more the patient finds himself/herself in a higher NYHA class,
the more the arrhythmia’s prevalence increases. The atrial fibrillation often represents a
worsening cause for the heart failure, and this worsening, by itself, generates atrial
fibrillation. A vicious cycle is created between heart failure and atrial fibrillation (Figure 3).
Figure 3 Vicious cycle between atrial fibrillation and heart failure. HF, heart failure; AF,
atrial fibrillation.
On the other hand we can still provide two positive news. The first one would be
that when possible, curing atrial fibrillation and restoring sinus rhythm, while improve the
clinical picture of the failing heart. The second is that the restoration of the normal rhythm
also improves the outcome of heart failure patients. For these and many more other
reasons we always need to do all that is possible in order to defeat atrial fibrillation.
Ventricular arrhythmias are represented by ventricular ectopic beats, accelerated
idioventricular rhythm, non-sustained ventricular rhythm, sustained ventricular tachycardia
and “the feared” ventricular fibrillation. These arrhythmias are identified during 24hr ECG
recordings or during continuous monitoring (telemetry monitoring systems) for hospitalized
patients (Figure 4).
Figure 4 Telemetry monitoring of a patient who develops during the hospitalization a short
run of non-sustained ventricular tachycardia.
Arrhythmias can be asymptomatic or may present themselves with palpitations,
light-headedness, dizziness, near-syncope, syncope or with even more severe symptoms
(refer to When symptoms don’t correspond to the disease…but at times they do). The
prevalence of these ventricular rhythm disturbances in heart failure patients is high, but
inferior to the atrial fibrillation one.
In most cases, arrhythmias (both atrial and ventricular) occur due to the same
underlying heart disease, but in other circumstances they can be only adverse effects of
drugs we use to treat this syndrome. I am referring to positive inotropic drugs like
catecholamines or phopshodiesterase inhibitors mainly used during acute heart failure
therapy, or dgitalis and diuretic used in chronic therapies as well. Needs to be mentioned
that diuretics do not present direct arrhythmogenic effects, but through electrolytic
disturbances (hypokalemia and/or hypomagnesemia) which can incur. On the other hand,
we also have drugs which can decrease arrhythmias’ incidence in cardiac failure: aside
from the proper anti-arrhythmic drugs, we have the betablockers, the statins, ACE
inhibitors and aldosterone antagonists.
Every day, in our electrophysiology lab, for patients with cardiac failure and rhythm
disturbances we apply particularly sophisticated techniques in order to eliminate the
negative effect of arrhythmias on the failing heart’s ventricular function, and to facilitate the
ventricles to work “more harmoniously” with each other.
Vladimir Guluta, MD