الفهرس 
Pathophysiology of ventricular dyssynchrony and mechanisms of CRTOnly 14 pages are availabe for public view
 |  | from | 82 |  |  |
| | | from | 82 | | |
Abstract
Heart failure is a common clinical syndrome which represents the end-stage of a number of several cardiac diseases. Which can result from many structural or functional cardiac disorders that impair the ability of the ventricle to fill with or eject blood.
Despite recent advances in drug treatment for heart failure (HF), many patients are not sufficiently improved by drug treatment. Previously, these patients could be offered only heart transplantation or a cardiac assist. Over the last twenty years the use of CRT has expanded and evolved considerably. The CRT proved its worth in improving the quality of life and reducing the symptoms of heart failure. There are many studies that have proven the long-term benefits of this device.
A significant number of heart failure patients have electromechanical desynchrony which increases their mortality rates. The known types of electromechanical desynchrony in a sequential manner are the atrioventricular delay, intraventricular delay, interventricular delay and intramural delay.
Cardiac resynchronization therapy improves mechanical LV function in patients with heart failure and ventricular desynchrony. Electrical resynchronization can decrease the LBBB-induced mechanical interventricular desynchrony between the right and the left ventricle and the intraventricular desynchrony within the left ventricle. Minimizing intraventricular desynchrony has been shown to improve global left ventricular function so that the cardiac resynchronization therapy increases cardiac output, decreases end systolic volume, and end diastolic volume also reduces mitral regurgitation, so that the hemodynamics of the heart are improved. Potential mechanisms of benefit include improved contractile function and reverse ventricular remodeling. Preliminary data from an experimental model suggest that CRT reduces regional and global molecular remodeling, generating more homogeneous activation of stress kinases and reducing apoptosis.
The acute mechanical effects of cardiac resynchronization therapy are accompanied by more chronic adaptations that lead to long-term benefit in the patients suffering from heart failure. Cardiac resynchronization therapy can improve the disturbed neurohormonal environment associated with chronic heart failure.
Since the introduction of cardiac resynchronization therapy (CRT) in 1994, this technique was developed quickly to be an established therapy. So the international guidelines recommended CRT as an appropriate therapy in selected patients.
In patients with New York Heart Association (NYHA) class III/IV disease in spite of adequate medical treatment, systolic heart failure and evidence of ventricular desynchrony by electrocardiography, CRT based on pacing the left ventricle (LV), both ventricles or multisided, improved quality of life and functional status, reduced heart failure-related hospitalizations and prolonged survival.
However, following current guidelines to identify the candidates for CRT, about 30–45%of CRT patients still lack improvement or even deteriorate (non-responders) during pacing.
Furthermore, the percentage of heart failure patients who might benefit but do not meet standard CRT indications is unknown. It has been documented that some patients have left ventricular asynchrony with congestive heart failure and normal QRS duration might respond to CRT. Thus, an improvement in patient selection for CRT is needed to optimize the outcome of this invasive and costly device.
There are many Factors affecting selection of patients for CRT. These factors help us to better select the patient who gets more benefits from CRT.
Studying these factors help us to know whether the patient is responder or non-responder, which help in better patient selection.
A careful evaluation of comorbidities and an estimate of life expectancy is recommended. A thorough pre-implant history and physical examination including review of vital signs and laboratory tests is recommended CRT candidates should have stable heart failure status on guideline-directed medical therapy prior to implant. A pre-implant comprehensive echocardiogram for quantification of LVEF and assessment of cardiac size and function is recommended. A pre-implant 12-lead ECG including QRS duration measure and characterization of QRS morphology is recommended. In patients at high thromboembolic risk on oral anticoagulant therapy with warfarin, continuing therapy at reduced dosage with close monitoring of INR is recommended perioperatively. Postoperative use of heparin is discouraged. Preoperative treatment with an antibiotic that has in vitro activity against staphylococci is recommended for infection prophylaxis.
A physical examination, device interrogation, chest X-ray, and surface ECG is recommended prior to discharge Careful attention to volume status is recommended after the implantation procedure as an acute response to CRT may include significant diuresis. A standard echocardiographic assessment is recommended prior to discharge if a procedural complication is suspected on the basis of patient symptoms or clinical findings. An assessment to assure 100%biventricular capture is recommended prior to discharge. The majority of patients implanted with CRT should remain in the hospital overnight after implant to observe clinical status.
Numerous parameters of intraventricular desynchrony have been suggested as predictors of potential responders to CRT. Mechanical desynchrony may be assessed using conventional M-mode and Doppler echocardiography. Newer modalities include tissue Doppler imaging (TDI), strain rate imaging (SRI), and tissue synchronization imaging (TSI).
The increase in EF and the decrease in LVESV were observed later after CRT. Benefits were observed regardless of the etiology of LV dysfunction, but the effects on ventricular function were less striking in patients with IHD. IVMD was an approximate guide to the probability of long-term improvement in cardiac structure and function in response to CRT.