Beta Blockers and Left Ventricular Dysfunction.

Remy

Administrator
So calcium channel blockers may help improve left ventricular dysfunction...I think this is the same thing that Lerner used to look at on an EKG as a biomarker and Cheney also observed in MECFS patients.

It makes sense because there has been a lot of chatter about channelopathies in MECFS.

http://www.cortjohnson.org/forums/threads/ion-channel-problems-found-in-me-cfs.2449/

Beta blockers can also help with dysautonomia and overactive sympathetic nervous system activation. Typically they are used in smaller doses than for typical cardiac purposes.

So anyone ever tried carvedilol?
Am J Cardiovasc Drugs. 2006;6(4):259-63.
Effects of nebivolol versus carvedilol on left ventricular function in patients with chronic heart failure and reduced left ventricular systolic function.

Lombardo RM1, Reina C, Abrignani MG, Rizzo PA, Braschi A, De Castro S.
Abstract

BACKGROUND:

Beta-adrenoceptor antagonist (beta-blocker) therapy results in a significant improvement in left ventricular (LV) systolic function and prognosis in patients with chronic heart failure. Both carvedilol and nebivolol produce hemodynamic and clinical benefits in chronic heart failure, but it is unknown whether their peculiar pharmacologic properties produce different effects on LV function.
OBJECTIVE:

To assess the effects on LV function of nebivolol compared with carvedilol in patients with chronic heart failure and reduced LV systolic function.
METHODS:

Seventy patients with a LV ejection fraction <or=40% and in New York Heart Association (NYHA) functional class II or III were randomly assigned to receive carvedilol or nebivolol therapy for 6 months. At baseline and after 6 months of treatment, all patients were assessed clinically and by biochemical and hematological investigation, ECG, 24-hour Holter monitoring, echocardiogram, measurement of ventilatory function, and a 6-minute walk test.
RESULTS:

Compared with baseline values LV end-systolic volume decreased and LV ejection fraction increased in both the carvedilol (from 79 +/- 38mL to 73 +/- 43mL and from 33% +/- 6% to 37% +/- 11%) and the nebivolol group (from 72 +/- 35mL to 66 +/- 32mL and from 34% +/- 7% to 38% +/- 10%), although the between-group differences were not statistically significant. ECG data showed a decrease in resting HR in both groups (from 83 +/- 20 bpm to 66 +/- 11 bpm for carvedilol and from 81 +/- 15 bpm to 65 +/- 11 bpm for nebivolol; p < 0.001 vs baseline for both groups) but no difference in the PQ, QRS, and QT intervals. Hematologic (in particular, N-terminal pro-brain natriuretic peptide), Holter monitoring (with the exception of HR), and respiratory functional data did not show any significant variation in either group after 6 months' therapy. SBP and DBP decreased in both groups. A small reduction in mean NYHA functional class from baseline was seen in both groups (from 2.5 +/- 0.5 to 2.2 +/- 0.5 for carvedilol [p < 0.05] and from 2.3 +/- 0.4 to 2.2 +/- 0.5 for nebivolol [not significant]). The 6-minute walk test showed a trend toward an increase in the walking distance in both groups. During 6 months of treatment no significant differences in adverse events were observed between the groups.
CONCLUSION:

Nebivolol is as effective as carvedilol in patients with symptomatic chronic heart failure and reduced LV systolic function.
 

Remy

Administrator
Looks like propranolol does not have the same effect on improvement of diastolic function.

http://circ.ahajournals.org/content/65/7/1337.full.pdf

Circulation. 1982 Jun;65(7):1337-50.
Effects of verapamil and propranolol on left ventricular systolic function and diastolic filling in patients with coronary artery disease: radionuclide angiographic studies at rest and during exercise.
Bonow RO, Leon MB, Rosing DR, Kent KM, Lipson LC, Bacharach SL, Green MV, Epstein SE.
Abstract
To determine the effects of verapamil on left ventricular (LV) systolic function and diastolic filling in patients with coronary artery disease (CAD), we performed gated radionuclide angiography at rest and during exercise in 16 symptomatic patients before and during oral verapamil therapy (480 mg/day). Twelve patients were also studied during oral propranolol (160--320 mg/day). LV ejection fraction at rest was normal in 13 patients, but abnormal diastolic filling at rest, defined as peak filling rate (PFR) less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 180 msec, was present in 15. During verapamil, resting ejection fraction decreased (control 50 +/- 10% [+/- SD), verapamil 45 +/- 12%, p less than 0.005), but resting diastolic filling improved: PFR increased (control 1.9 +/- 0.6 EDV/sec, verapamil 2.3 +/- 0.9 ECV/sec, p less than 0.005) and time to PFR decreased (control 185 +/- 38 msec, verapamil 161 +/- 27 msec, p less than 0.05). Exercise ejection fraction did not change during verapamil (control 42 +/- 13%, verapamil 43 +/- 12%, NS), but exercise PFR increased (control 3.1 +/- 0.9 EDV/sec, verapamil 3.6 +/- 1.1 EDV/sec, p less than 0.05) and exercise time to PFR decreased (control 108 +/- 30 msec, verapamil 91 +/- 17 msec, p less than 0.05). In contrast, propranolol did not alter ejection fraction, PFR, or time to PFR at rest or during exercise. Thus, LV ejection fraction is decreased by verapamil at rest but is unchanged during exercise. While LV systolic function is not improved by verapamil, LV diastolic filling is enhanced by verapamil, both at rest and during exercise. These mechanisms may account in part for the symptomatic improvement in many patients during verapamil therapy.
 

Strike me lucky

Well-Known Member
I googled atrial fibrillation in cfs me, not that i know i have it yet but hr monitor is irregular . Lerners work came up and mentioned heart wall abnormalities??I cant recall,3am here at moment.

Im using metoprolol and it calms things down but i do feel abit sedated on full dose, half is ok
 

Remy

Administrator
I googled atrial fibrillation in cfs me, not that i know i have it yet but hr monitor is irregular . Lerners work came up and mentioned heart wall abnormalities??I cant recall,3am here at moment.

Im using metoprolol and it calms things down but i do feel abit sedated on full dose, half is ok
I need to go back and read what Lerner wrote about left ventricular dysfunction. I think there was some characteristic pattern on an EKG? But I was never really all that clear on it and I'm not 100% this is the same thing, though it sure sounds like it!
 

Strike me lucky

Well-Known Member
I need to go back and read what Lerner wrote about left ventricular dysfunction. I think there was some characteristic pattern on an EKG? But I was never really all that clear on it and I'm not 100% this is the same thing, though it sure sounds like it!

I recall he was mostly on about flat t waves and never seen af mentioned until a recent article. But referred it to a type of heart failure he sees in cfsers with ebv/cmv which is reversible with av treatment???
 

Remy

Administrator
The book, Treatment of Chronic Fatigue Syndrome in The Antiviral Revolution Era, has this to say, based on Lerner's work,

The research conducted revealed that all CFS patients have abnormal oscillating T-wave flattenings and T-wave inversions detectable from twenty four hour electrocardiographic (Holter) monitoring...Notably, chronic diseases such as hypertensive vascular disease, electrolyte abnormalities, and coronary artery disease may produce similar oscillating abnormal T-waves. However, since people suffering from CFS are generally young, such chronic diseases rarely afflict CFS sufferers and can thus be excluded as the causative agent.
Also:

An initial group of CFS patients also demonstrated abnormal left ventricular dynamics characterized by a decreased or falling ejection fraction, abnormal wall motion, or dilatation by radionuclide stress multiple gated acquisition (MUGA) studies.
Still don't really understand though.
 

Strike me lucky

Well-Known Member
The book, Treatment of Chronic Fatigue Syndrome in The Antiviral Revolution Era, has this to say, based on Lerner's work,



Also:



Still don't really understand though.
Sèems the ticker just isnt producing strong ventricle contractions, so less blood replenishing oxygen to cells. Could also be a factor in pots if one has pooling of blood in the legs as the heart needs a certain volume of blood in the ventricles to contract properly???
 

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