• IMA sites
  • IMAJ services
  • IMA journals
  • Follow us
  • Alternate Text Alternate Text
עמוד בית
Mon, 06.05.24

Search results


January 2006
S. Silberman, A. Oren, M. W. Klutstein, M. Deeb, E. Asher, O. Merin, D. Fink, D. Bitran.

Background: Ischemic mitral regurgitation is associated with reduced survival after coronary artery bypass surgery.

Objectives: To compare long-term survival among patients undergoing coronary surgery for reduced left ventricular function and severe ischemic MR[1] in whom the valve was either repaired, replaced, or no intervention was performed.

Methods: Eighty patients with severe left ventricular dysfunction and severe MR underwent coronary bypass surgery. The mean age of the patients was 65 years (range 42–82), and 63 (79%) were male. Sixty-three (79%) were in preoperative NYHA functional class III-IV (mean NYHA 3.3), and 26 (32%) were operated on an urgent/emergent basis. Coronary artery bypass surgery was performed in all patients. The mitral valve was repaired in 38 and replaced in 14, and in 28 there was no intervention. The clinical profile was similar in the three groups, although patients undergoing repair were slightly younger.

Results: Operative mortality was 15% (8%, 14%, and 25% for the repair, replacement and no intervention respectively; not significant). Long-term follow up was 100% complete, for a mean of 38 months (range 2–92). Twenty-nine patients (57%) were in NYHA I-II (mean NYHA 2.3). Among the surgery survivors, late survival was improved in the repair group compared to the other groups (P < 0.05). Predictors for late mortality were non-repair of the mitral valve, residual MR, and stroke (P = 0.005).

Conclusions: Patients with severe ischemic cardiomyopathy and severe MR undergoing coronary bypass surgery should have a mitral procedure at the time of surgery. Mitral valve repair offers a survival advantage as compared to replacement or no intervention on the valve. Patients with residual MR had the worst results.






[1] MR = mitral regurgitation


June 2005
M. Arad, H. Lahat and D. Freimark
 Familial cardiomyopathies represent a substantial portion of idiopathic dilated cardiomyopathy in clinical practice. Diversity of clinical presentations and variability in penetrance lead to under-recognition of this disease entity as an inherited disorder. The mechanisms by which mutations in different genes perturb cardiac function and lead to pathologic remodeling help understand the molecular pathways in disease pathogenesis and define the potential targets for therapeutic interventions. Appreciating when DCM[1] is inherited might spare unnecessary diagnostic efforts and, instead, help give appropriate attention to the timely detection of subclinically affected family members. Establishing preventive therapy in asymptomatic family members showing early signs of cardiac dysfunction might prevent death and slow down progression to end-stage heart failure.


 





[1] DCM = dilated cardiomyopathy


January 2003
E. Zalzstein, A. Wagshal, N. Zucker, A. Levitas, I.E. Ovsyshcher and A. Katz
March 2002
Edward G. Abinader, MD FRCPI, Dawod Sharif, MD, Arie Shefer, MD and Johanan Naschitz, MD

Background: Long-term follow-up in apical hypertrophic cardiomyopathy is rare.

Objective: To study the natural history of the disease.

Methods: We followed 11 patients, 5 women and 6 men, for 5-20 years.

Results: At presentation all 11 patients had typical features of apical hypertrophic cardiomyopathy, with dyspnea in 3 and chest pains in 8, of whom 5 were typical of angina and 3 had myocardial infarction. R-wave voltage and T-wave negativity progressively decreased in magnitude at serial electrocardiograms in four patients. Perfusion defects were detected on thallium myocardial scintigraphy in three, increased apical uptake in two, and normal in one patient. Apical aneurysm with normal coronary arteries developed in a patient who had sustained ventricular tachycardia. All of the 10 catheterized patients had normal coronaries except for one with significant left anterior descending artery stenosis and another with a minor lesion. Symptomatic sustained ventricular tachycardia was found in two patients, one of whom required the implantation of an internal cardioverter-defibrillator.

Conclusions: Apical hypertrophic cardiomyopathy may develop morphologic and electrocardiographic changes with life-threatening arrhythmias necessitating close follow-up and treatment.

February 2002
Diab Mutlak, MD, Luis Gruberg, MD, Shimon Reisner, MD and Walter Markiewicz, MD, FACC

Background: Percutaneous transluminal septal ablation was recently introduced as an alternative to surgical treatment of hypertrophic obstructive cardiomyopathy. In this procedure, alcohol is injected into a proximal septal artery to create a localized myocardial infarction.

Objectives: To characterize the immediate and mediumterm results following PTSMA.

Methods: Of 13 patients referred for PTSMA, 8 were found suitable for the procedure. Hemodynamic parameters were evaluated prior to and following the procedure, and clinical and echo-Doppler parameters at 2 weeks and 9 months later.

Results: The procedure was technically successful in all patients. Resting left ventricular outflow gradient at rest (by Doppler) fell from 82 + 37 to 15 + 8 mmHg (P<0.001) 9 months later. Late post-procedural gradient after the Valsalva maneuver was 2 + 24 mmHg. The degree of mitral regurgitation fell from 2.0 + 0 to 1.5 + 0.5 (P<0.05). New York Heart Association class for dyspnea improved from 2.8 + 0.5 to 1.8 + (P<0.01) and Canadian Cardiovascular Society class for angina from 2.0 + 1.3 to 1.3 + 1.2 (P=0.08). Complete right bundle branch block developed in six patients, temporary complete atrioventricular block in three, and persistent block requiring permanent pacing in one. No flow in the distal left anterior descending coronary artery (presumably due to spilling of alcohol) was seen in one (with development of a small antero-apical infraction) and ventricular fibrillation 2 hours post-procedure in one. None of the patients died.

Conclusion: PTSMA provided a substantial reduction in left ventricular outflow gradient associated with an improvement in symptomatology. Serious complications are not uncommon. Long-term follow-up is unknown.
 

April 2000
Shahar Zimand, MD, Patricia Benjamin, Mira. Frand, MD, David Mishaly, MD and Julius Hegesh, MD
Legal Disclaimer: The information contained in this website is provided for informational purposes only, and should not be construed as legal or medical advice on any matter.
The IMA is not responsible for and expressly disclaims liability for damages of any kind arising from the use of or reliance on information contained within the site.
© All rights to information on this site are reserved and are the property of the Israeli Medical Association. Privacy policy

2 Twin Towers, 35 Jabotinsky, POB 4292, Ramat Gan 5251108 Israel