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Updated January 25, 2007
November 2, 2005 - Doctors often do not prescribe resistance training (like lifting weights) for fear it may somehow overstress the heart muscle. These researchers studied how 8 weeks of resistance training affected the hearts of 8 male CHFers, while 7 CHFers were a control group not exercising.
Before and after 8 weeks of training, patients had a resting echo to measure their end-diastolic (EDD) and end-systolic dimensions (ESD), their EF, fractional shortening (FS) and stroke volume (SV). During the 8 weeks of resistance training, no bad effects on LV measurements were seen.
After 8 weeks of resistance training, EF and FS of the exercising patients was significantly higher than in control patients. EF was 11% higher and FS was 8% higher in exercising patients. Now doctors should realize that resistance training is not only safe for CHFers but also improves them physically. The researchers recommend adding resistance training to cardiac rehab for people with heart failure.
Title: The effect of resistance training on left ventricular function and structure of patients with chronic heart failure.
Authors: Itamar Levingera, Roger Bronksa, David V. Codyb, Ian Lintonb, Allan Daviea.
Source: Int J Cardiol 2005;105:159-163.
November 22, 2005 - BMI (body mass index) is a measure of obesity. The higher the BMI, the fatter you are. As BMI increases, BNP blood test results take on different meaning. A very fat CHFer may have a lower BNP result and still have serious heart failure. This study suggests that instead of saying you have heart failure at 100 pg/ml or higher, very fat people may have CHF at 54 pg/ml and higher.
To find out what BNP level would identify 90% of patients with different body weights who had CHF, researchers studied 1,368 patients who were enrolled in the BNP Multinational Study. These patients went to an ER for shortness of breath. BNP was measured on arrival, and two cardiologists (who did not know the BNP results [blinded]) confirmed a HF diagnosis based on various factors, including x-rays, echos, history and physical exams, and all lab work except BNP - after a BNP test was done.
Patients were divided into 3 categories based on BMI: In severely obese patients, a cut-off of 54 pg/mL detected 90% of patients in CHF in this study. In all patients not seriously obese, a cut-off point of 100 pg/ml accurately predicted heart failure.
This study shows how important it is to consider all factors in diagnosing CHF, including BNP, x-ray, echo, physical exam and more.
Source: AHA 2005 Scientific Sessions: Abstract 3512. Presented 11/16/2005.
March, 2006 - Lead researcher Dr. William Abraham is planning a phase 3 trial of lixivaptan after a phase 2 trial gave good results. Okay, let's start at the beginning. Vasopressin is a hormone called an anti-diuretic. It makes your kidneys hang onto water. So with heart failure, too much vasopressin increases edema - a bad thing. Lixivaptan is a "V2 receptor arginine vasopressin antagonist." I'm gonna call it a "vasopressin blocker" even though doctors are calling them AVPs.
You know how Coreg blocks both beta-1 and beta-2 receptors, while Toprol-XL blocks just beta-1 receptors. Lixivaptan is a V2 blocker because it blocks vasopressin 2 receptors.
Right now, we CHFers take diuretics like furosemide and torsemide (Lasix and Demadex) to make the kidneys let go of sodium - all that water we pee out with the sodium is really just along for the ride. Actually, we're peeing out much more than water, including potassium, magnesium, sodium and other substances our bodies need. In fact, low blood sodium levels mean our risk of death is quite a bit higher than with normal blood sodium levels.
Lixivaptan gets your kidneys to remove all that extra fluid without removing the potassium, magnesium, sodium, etc. That's a huge benefit. This phase 2 trial included 42 class two to class 3 CHFers who all needed diuretics.In the phase 2 trial, CHFers drank no fluid overnight, then took a placebo (12 patients), or lixivaptan at doses of 10mg, 30mg, 75mg, 150mg, 250mg, or 400mg (5 patients per dose) on day one, followed by 4 hours of continued fluid restriction. Then patients could drink when they wanted.
At every dose but the lowest (10 mg), lixivaptan significantly increased urine output over 4 hours compared to placebo. Over 24 hours, output was about 2 liters for placebo patients versus 4 liters in patients taking 400 mg of lixivaptan. The amount of sodium removed along with the liquid in lixivaptan patients was much less (called solute-free water excretion). Now, this is obviously good news to us CHFers. It also shows that vasopressin plays an important role in CHF edema.
These kind of drugs are called "aquaretics." They include conivaptan, lixivaptan, tolvaptan, and one just called SR-121463 as far as I know. Added to diuretics, they may really help us get rid of extra fluid without increasing risk from losing electrolytes too. They may also help CHFers who don't respond well to regular diuretics.
Source: Ohio State University Medical Center. Editor: Emily Caldwell. Source: J Am Coll Cardiol, 2006; 47:1615-1621, doi:10.1016/j.jacc.2005.11.071 (Published online 24 March 2006).
Title: Aquaretic Effect of Lixivaptan, an Oral, Non-Peptide, Selective V2 Receptor Vasopressin Antagonist, in New York Heart Association Functional Class II and III Chronic Heart Failure Patients.
Authors: William Abraham, Alireza Shamshirsaz, Kim McFann, Ron Oren, Robert Schrier.
PMID: 16630999. Source: Congest Heart Fail. 2006 Jan-Feb;12(1):55-60. 12;1:55.
Title: Hyponatremia and heart failure--treatment considerations.
Author: Sica DA.
Source: Am J Med. 2006 Jul;119(7 Suppl 1):S87-92.
Title: Vasopressin antagonists as aquaretic agents for the treatment of hyponatremia.
Author: Palm C, Pistrosch F, Herbrig K, Gross P.
August 25, 2006 - Alcohol septal ablation (ASA) gives continued improvement in diastolic function for hypertrophic cardiomyopathy patients. This trial shows that diastolic improvement lasts at least 2 years after the procedure. Harvard researchers measured diastolic function by echo at study start, and at one and two-year follow-ups after ASA in 30 HCM patients.
Functional heart class improved from class 3 to class 1-1/2 at one year and to class one at 2 years after the procedure. ASA also improved average LV outflow tract gradients from 75 to 19 mmHg at one year, with the improvement remaining at 2 years. All 30 patients had diastolic dysfunction at study start.
Source: Eur Heart J 2006;27:1805-1810.
Authors: Yoerger, Danita, et all.
Source: Reuters Health
September 1, 2006 - Researchers studied whether transplanting patients' own adult bone marrow mononuclear cells (BMMCs) into those patients' hearts gave any benefit. All patients had CHF that did not respond well to standard treatment. Twenty-eight CHFers were include. Fourteen got standard CHF meds plus BMMC transplant and 14 got standard meds only (control patients).
BMMCs were harvested from the 14 CHFers. Physical exam results, test results, rhythm studies, echos, and PET scans were recorded. The 14 patients getting stem cells had improved CHF symptoms within 3 days. EF increased by 9% one week later and 11% 3 months after the procedure compared to study start.
Left heart end-systolic volume went down 31% after 3 months. BNP level at day 3 after cell implant went way down by 69% and 7 days afterward by 70%, while ANP levels went up by 30% at day - all good 7. PET scans showed a significant increase in cell activity of 10% in the areas affected by heart attack.
No patient died in the treated group by 6-month follow-up. In contrast, heart failure did not improve in any control patient. EF went down in control patients by 7% after 3 months. Two control patients died from CHF in 6 months. This human trial shows that in-the-heart BMMC transplant is safe and effective for reducing symptoms, increasing heart function, and possibly prolonging life in patients with end-stage heart failure that does not respond to standard therapy.
Source: Am J Cardiol. 2006 Sep 1;98(5):597-602. Epub 2006 Jun 30.
Title: Effect of intracoronary transplantation of autologous bone marrow-derived mononuclear cells on outcomes of patients with refractory chronic heart failure secondary to ischemic cardiomyopathy.
Authors: Gao LR, Wang ZG, Zhu ZM, Fei YX, He S, Tian HT, Zhang NK, Chen Y, Xu HT, Yang Y.
September, 2006 - Trimetazidine is actually a free fatty acid (FFA) oxidation inhibitor, which I will call an FFA-blocker. Trials in Europe and Asia suggest it improves left heart function and heart class. Trimetazidine is approved in those areas for angina treatment.
Trimetazidine has anti-ischemic properties - that means it helps the heart sustain high-enough blood/oxygen levels. However, this drug does not affect oxygen consumption. The drug reduces cell acidosis, calcium overload and free-radical injury that leads to ischemia. It changes the heart's energy production from FFA use to glucose use, so left heart function is preserved.
Researchers gave 28 CHFers 20mg trimetazidine 3 times a day plus standard CHF drugs and gave 27 CHFers standard treatment only. Average follow-up was 13 months. At study start all CHFers had exercise and echo tests. EF and heart class were measured.
In trimetazidine patients, heart class improved versus standard therapy patients. Trimetazidine improved left heart volume (a good thing) from an average of 98ml to 81ml, and increased EF from 36 to 43%. In standard therapy patients, left heart end-diastolic volume increased from an average 142ml to 156ml and systolic volume from 86ml to 104ml. EF in standard therapy patients went down from an average of 38 to 34%.
Trimetazidine appears to protect the heart from the bad effects of ischemia, and it improves the heart's pumping strength in CHFers with hibernating cells - hibernating means heart muscle cells that aren't currently working but aren't dead and might work again over time).
CHF worsens quality and length of life more in those with diabetes. Trimetazidine, reduces fatty acid beta-oxidation (a type of energy source for the heart), so the heart uses the sugar pathway for its energy instead. This change helps the heart function better in diabetics
Researchers studied heart function after one month of trimetazidine (Vastarel) added on to standard therapies for type 2 diabetics with CHF. Twenty diabetic patients with ischemic heart failure were involved. Their average age was 66 years and their average heart class was 2 to 3. They took trimetazidine (60mg daily) or placebo in a double-blind crossover design, meaning they first added the drug, then the placebo or the other way around, with no one involved knowing which order was used in each CHFer. Exercise tolerance, echo, and tissue doppler imaging were done both at rest and exercise before and during treatment.
Exercise tolerance did not change in either group. EF at rest and moderate exercise only improved with trimetazidine during the first treatment period. TDI measures did not change much during treatment. In this early trial, there were only weak signs of improved heart output at rest and during exercise. More research is needed in diabetic CHFers.
Source: Reuters Health Source: J Am Coll Cardiol. 2006 Sep 5;48(5):992-8. Epub 2006 Aug 17.
Comment in: J Am Coll Cardiol. 2006 Sep 5;48(5):999-1000.
Title: A randomized clinical trial of trimetazidine, a partial free fatty acid oxidation inhibitor, in patients with heart failure.
Authors: Fragasso G, Palloshi A, Puccetti P, Silipigni C, Rossodivita A, Pala M, Calori G, Alfieri O, Margonato A.
Source: Am J Cardiol. 2006 Sep 4;98(5A):19J-24J. Epub 2006 Jul 24.
Title: Role of trimetazidine in management of ischemic cardiomyopathy.
Authors: Bertomeu-Gonzalez V, Bouzas-Mosquera A, Kaski JC
Source: J Cardiovasc Pharmacol. 2004 Jul;44(1):101-8.
Title: Effects of trimetazidine on left ventricular function in patients with type 2 diabetes and heart failure.
Authors: Thrainsdottir IS, von Bibra H, Malmberg K, Ryden L.
January, 2007 - Can CHFers with a narrow QRS interval (less than 120 ms) benefit from CRT (BiV pacemaker)? Using an echo to measure how well the heart's 4 chambers beat together as a team during systole can show if dysynchrony exists. If it does, a BiV pacemaker will probably help.
Researchers studied 102 class 3 and class 4 CHFers. Fifty-one had wide QRS (greater than 120 ms) and 51 had narrow QRS (less than 120 ms). A form of echo called TDI (Tissue Doppler Imaging) was used to find those CHFers with systolic dysynchrony. Echos were done at study start and 3 months after CRT began.
Systolic LV volume significantly improved in all CRT patients - both narrow-QRS patients and wide-QRS patients.. All CRT patients improved in heart class, ability to exercise (Vo2max), 6-minute walk distance, EF, and mitral valve leakage.
CRT was then turned off (the pacemaker turned off) for 4 weeks. Benefits were then lost but regained when CRT pacing was restarted. Biventricular pacing in CHFers with narrow QRS intervals and dysynchrony as shown on echo do benefit. Their benefit is as great as in CHFers with wide QRS and dysynchrony.
Other researchers also studied CRT use. They studied CHFers with both narrow QRS interval and LV dysynchrony as shown by TDI. Thirty-three consecutive CHFers with narrow QRS intervals and 33 other consecutive CHFers with wide QRS were included. All had LV dysynchrony measured by TDI. All were class 3 or class 4, and had EF less than 36%.
QRS at study start had nothing to do with LV dyssynchrony. Both narrow-QRS and wide-QRS patients had similar improvements in symptoms, LV improvement, and heart class, which improved by a full class in all CRT patients. Average LV end-systolic volume improved 39 ml in narrow-QRS patients and 44 ml in wide-QRS patients.
Researchers have also shown that TDI done by different technicians on different kinds of echo machines all give reliable results in showing dysynchrony. This means it can be spotted at most medical centers and cardiologist offices if doctors and techs are on the ball - very good news for us CHFers. Now using echo (TDI) to spot dysychrony seems much more important then QRS interval to see which CHFers will benefit from BiV pacemakers.
Source: J Am Coll Cardiol. 2006 Dec 5;48(11):2251-7.
Title: Benefits of cardiac resynchronization therapy for heart failure patients with narrow QRS complexes and coexisting systolic asynchrony by echocardiography.
Authors: Yu CM, Chan YS, Zhang Q, Yip GW, Chan CK, Kum LC, Wu L, Lee AP, Lam YY, Fung JW.
Source: Echocardiography. 2007 Jan;24(1):40-6.
Title: Reliability of echocardiographic indices of dyssynchrony.
Authors: Gabriel RS, Bakshi TK, Scott AG, Christiansen JP, Patel H, Wong SP, Armstrong GP.
Source: J Am Coll Cardiol. 2006 Dec 5;48(11):2243-50. Epub 2006 Nov 9.
Title: Cardiac resynchronization therapy in patients with a narrow QRS complex.
Authors: Bleeker GB, Holman ER, Steendijk P, Boersma E, van der Wall EE, Schalij MJ, Bax JJ.
October 18, 2006 - Researchers studied inhaled treprostinil for severe PH by measuring its effects on blood flow and gas exchange in the lungs. Although inhaled iloprost helps PH patiens, it requires 6 to 9 inhaling sessions per day. Treprostinil lasts longer in the body when inhaled.
Three different studies were done including 123 patients using right heart cath. The main endpoint was change in PVR. Average lung artery pressure was about 50 mmHg in all three studies.
Researchers also studied inhaling treprostinil in PH patients already taking oral bosentan. Twelve PH patients with symptoms despite taking bosentan got either 30 microgams of inhaled treprostinil 4 times a day (6 patients) or 45 micrograms 4 times a day (6 patients), again using an ultrasonic nebulizer.
Six-minute walk distance, heart class, and blood flow were measured at study start and again at 12 weeks. One patient dropped out due to another health problem. In the other 11 patients, inhaled treprostinil was safe and well tolerated.
Inhaled treprostinil increased 6-minute walk distance from 339 meters to 406 meters at 12 weeks. Only one patient taking 30 micrograms improved walk distance but 5 of 6 patients taking 45 micrograms improved. Over 12 weeks, average pulmonary artery pressure improved 10% and pulmonary vascular resistance improved 26%. Heart class improved from class 3 to class two in 9 of 11 patients.
Inhaled treprostinil seems safe and effective for improving exercise ability, heart class, and lung function in PH patiens with symptoms already taking bosentan.
Source: J Am Coll Cardiol. 2006 Oct 17;48(8):1672-81. Epub 2006 Sep 26.
Title: Favorable effects of inhaled treprostinil in severe pulmonary hypertension: results from randomized controlled pilot studies.
Authors: Voswinckel R, Enke B, Reichenberger F, Kohstall M, Kreckel A, Krick S, Gall H, Gessler T, Schmehl T, Ghofrani HA, Schermuly RT, Grimminger F, Rubin LJ, Seeger W, Olschewski H.
Source: J Am Coll Cardiol. 2006 Oct 3;48(7):1433-7. Epub 2006 Sep 14.
Title: Safety and efficacy of inhaled treprostinil as add-on therapy to bosentan in pulmonary arterial hypertension.
Authors: Channick RN, Olschewski H, Seeger W, Staub T, Voswinckel R, Rubin LJ.
All information on this site is opinion only. All concepts, explanations, trials, and studies have been re-written in plain English and may contain errors. I am not a doctor. Use the reference information at the end of each article to search MedLine for more complete and accurate information. All original copyrights apply. No information on this page should be used by any person to affect their medical, legal, educational, social, or psychological treatment in any way. I am not a doctor. This web site and all its pages, graphics, and content copyright © 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004, 2005, 2006, 2007 Jon C.