About one third of patients with heart failure (HF) do not benefit appreciably or respond to cardiac resynchronization treatment (CRT). Some other have a clinical benefit with physiological confirmation in the form of echocardiographic demonstration of reduction in heart size and increase in the ejection fraction. A relatively small subset show a marked improvement both symptomatically and in terms of impressive improvement in terms of ejection fraction and reduction in left ventricular size.
Neither EKG nor echocardiographic patterns accurately predict who will respond and to what degree. However, patients with a LBBB EKG pattern -particularly using the new criteria suggested by Strauss (1 )- are much more likely to have a favorable response. In fact CRT basically "treats" the electric and associated mechanical dyssynchrony imposed by the left bundle branch block.Some of the variables influencing response include how much myocardial damage may have already occurred in the patient ( e.g. heart attacks) and the location of the left ventricular lead in relationship to left ventricular scar(s).
The most dramatic example of super responders was reported by Vaillent et al in 2013. (2). They described 6 patients with a diagnosis of LBBB without evidence of coronary or other heart disease and an EJ of greater than 50% at the time of diagnosis. Over a period of five to 21 years all developed heart failure severe enough to warrant referral for CRT. Following CRT, ejection fraction improved greatly , five of the six within 3 months .Mean EJ increased from 31 to 56.In one patient , from 26 to 60.Other cardiac functional indices improved as well
The authors suggest that these cases "strongly support the concept of LBBB-induced cardiomyopathy".This idea was apparently suggested earlier by Blanc et al in 2005 (4)
LBBB induced heart failure represents a vary small percentage of patient who are treated with CRT. Ghani et al (3) report on the predictors of long term outcome of "super-responders to CRT which they define as Left ventricular EF (LVEF) greater than 50% ( mean of 54.9%, +/-6) on follow-up echocardiogram.The group whose EF was between 30 and 50% were labelled as "responders"
They describe 56 patients from a group of 347 patients with primary CRT D indication. The predictors were female sex,nonischemic etiology,higher EF at baseline and wider QRS duration.
Vaillant's patients , when compared to Ghani's patient, perhaps could be considered "super super" responders.
1. Strauss DG et al, Defining Left Bundle Branch block in the Era of Cardiac Resynchronization Therapy. American J Cardiology 2011,Vol 107 pg 927-934
2. Vaillant C et al. Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J. Amer College of Cardiology 2013,vol 61, p 1089
3. Ghani, S et al Predictors and long term outcome of super-responders to cardiac resynchronization therapy. Clin Cardiology 2017
4.Blanc J et al. Evaluation of left bundle branch lock as a reversible cause of non-ischemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace 2005;7,604
Thursday, March 23, 2017
Sunday, March 19, 2017
Do low levels of cardiovascular fitness predispose to cardiac hypertrophy?
There is evidence that suggests low levels of cardiac fitness predispose to maladaptive cardiac remodeling typically manifest as concentric remodeling and concentric hypertrophy and increased ventricular stiffness and diastolic dysfunction.
Lovic and Kokkinos and co workers correctly point out that the cardiac hypertrophy consequent to high blood pressure differs from the typical physiological cardiac hypertrophy of the endurance athlete realizing that extreme examples of the latter can be difficult to distinguish from the former.
Lovic et al makes the following argument in a 2016 issue of the Journal of Hypertension.
Low fitness level individuals will reach a systolic blood pressure of 150 at low levels of exercise, e.g. 4-5 METS , which are levels commonly encountered in some activities of everyday living.
150 systolic blood pressure is necessary to trigger cardiac remodeling. Individuals, who are more fit, are able to do that level of work without that degree of BP rise. So individuals with low fitness may spend considerable time each day with a BP of sufficient magnitude to trigger hypertrophic changes in the left ventricle, even though their BP as measured in their doctor's office may be normal.
Their data (1) found an inverse relationship between exercise capacity, blood pressure response to exercise and left ventricular mass.Further, they have published data that showed 16 weeks of aerobic training resulted in subjects having a significantly lower blood pressure level when they exercised at the every day activity level of 3-5 METS. A reduction in previously elevated left ventricular mass was also shown.
Other data consistent with this notion comes from a study by Brinker et al ( 2) from Southwestern Medical School in Dallas. They studied subjects aged 42 -67 years of age with stress testing and echocardiography. Those individuals in the lowest fitness category ( they divided the group into 3 fitness levels ) had 40 % concentric hypertrophy as well as a 9% prevalence of diastolic dysfunction ( as defined by the e/a ratio on mitral valve echo flow studies)
Data from the Dallas group and others have outlined the concept of there being two distinct cardiac phenotypes related to the development of both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).They are:
1)Subclinical systolic dysfunction (EF may be normal but abnormalities detectable by measurement of global strain with speckle echocardiography)),with eccentric cardiac hypertrophy with increased LV diameter)-the proposed precursor to HFrEF
2)Subclinical diastolic dysfunction with concentric LV hypertrophy; with increased relative wall thickness (RWT) -the proposed precursor to diastolic heart failure (HFpEF)
Increasing data strongly suggest that low fitness levels predispose to the precursors of HFpEF.
Lovic's work suggesting that exercise induced elevated blood pressure in the unfit during the usual daily activities may be one possible mechanism involved.
1)Lovic, D et al Left ventricular hypertrophy in athletes and hypertensive patients.J Clin Hypertension 2017,
2) Brinker SK et al. An association of Cardiorespiratory Fitness with left ventricular remodeling and diastolic dysfunction. JACC Heart Failure., Vol 2, no 3, 2014, p 238
5/1/17 An embarrassingly large number of typos and misspellings were corrected and again on 5/16/17.
Lovic and Kokkinos and co workers correctly point out that the cardiac hypertrophy consequent to high blood pressure differs from the typical physiological cardiac hypertrophy of the endurance athlete realizing that extreme examples of the latter can be difficult to distinguish from the former.
Lovic et al makes the following argument in a 2016 issue of the Journal of Hypertension.
Low fitness level individuals will reach a systolic blood pressure of 150 at low levels of exercise, e.g. 4-5 METS , which are levels commonly encountered in some activities of everyday living.
150 systolic blood pressure is necessary to trigger cardiac remodeling. Individuals, who are more fit, are able to do that level of work without that degree of BP rise. So individuals with low fitness may spend considerable time each day with a BP of sufficient magnitude to trigger hypertrophic changes in the left ventricle, even though their BP as measured in their doctor's office may be normal.
Their data (1) found an inverse relationship between exercise capacity, blood pressure response to exercise and left ventricular mass.Further, they have published data that showed 16 weeks of aerobic training resulted in subjects having a significantly lower blood pressure level when they exercised at the every day activity level of 3-5 METS. A reduction in previously elevated left ventricular mass was also shown.
Other data consistent with this notion comes from a study by Brinker et al ( 2) from Southwestern Medical School in Dallas. They studied subjects aged 42 -67 years of age with stress testing and echocardiography. Those individuals in the lowest fitness category ( they divided the group into 3 fitness levels ) had 40 % concentric hypertrophy as well as a 9% prevalence of diastolic dysfunction ( as defined by the e/a ratio on mitral valve echo flow studies)
Data from the Dallas group and others have outlined the concept of there being two distinct cardiac phenotypes related to the development of both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).They are:
1)Subclinical systolic dysfunction (EF may be normal but abnormalities detectable by measurement of global strain with speckle echocardiography)),with eccentric cardiac hypertrophy with increased LV diameter)-the proposed precursor to HFrEF
2)Subclinical diastolic dysfunction with concentric LV hypertrophy; with increased relative wall thickness (RWT) -the proposed precursor to diastolic heart failure (HFpEF)
Increasing data strongly suggest that low fitness levels predispose to the precursors of HFpEF.
Lovic's work suggesting that exercise induced elevated blood pressure in the unfit during the usual daily activities may be one possible mechanism involved.
1)Lovic, D et al Left ventricular hypertrophy in athletes and hypertensive patients.J Clin Hypertension 2017,
2) Brinker SK et al. An association of Cardiorespiratory Fitness with left ventricular remodeling and diastolic dysfunction. JACC Heart Failure., Vol 2, no 3, 2014, p 238
5/1/17 An embarrassingly large number of typos and misspellings were corrected and again on 5/16/17.
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