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Heart Disease (Expert Forum)
What is the stuff about hypokenisis, perfusion defect, ejection fraction, and
This forum is for questions and support regarding heart issues such as: Angina, Angioplasty, Arrhythmia, Bypass Surgery, Cardiomyopathy, Coronary Artery Disease, Defibrillator, Heart Attack, Heart Disease, High Blood Pressure, Mitral Valve Prolapse, Pacemaker, PAD, Stenosis, Stress Tests.
What is the stuff about hypokenisis, perfusion defect, ejection fraction, and
by dwolfe, Aug 07, 2005 12:00AM
First of all, a little history from my reports.
Ischemic cardiomyopathy, CAD, MI, Cardiac arrest; inductable vtach, chronic angina, atrial fib, ventricular fib, dislipidemia, syncope, sick sinus syndrome, severe hypokinesis of the anterior wall, anterior septal wall, and the left ventricular apex. Also a marked anterior, septal, and apical perfusion defect with absent tracer uptake extending form the basil to the distal left ventricular segments which revealed no evidence of redistribution on the delayed images.
LVEF of between 20% and 35% according to which test and when. Pulmonary artery systolic pressure estimated at 44 mmHg consistent with pulmonary hypertension.
8/26/03 I was told after MI that I only had a 10% plaque in my arteries and nothing was done until it reached at least 50%.
01/18/04 Second MI was called acute with total blockage of one of the arteries. Reports also say I was in cardiogenic shock. Have a large scar on my anterior wall. EF 18-22%.
3/30/05 Third and fourth attacks were more like passing out. The first of these I didn’t tell anyone and the second my wife found me approximately 15 minutes after it started and thought I was having a seizure along with a heart attack. Anyway, back to the hospital and I am told I have ventricular fib, ventricular tycardia, sick sinus syndrome, and syncope and they put in a defibulator. EF 30-36%
7/26/05 Had another stress test done. Poor heart rate recovery, 1mm upsloping ST segment depression, lv dialated with evidence of severe hypokinesis to akinesis of the anterior wall, interventricular septum, distal inferior wall, distal lateral wall, and left ventricular apex. EF 25%
7/26/05Then I go to my regular doctor later to get a shoulder problem looked at and my wife made him give me a ct scan because I forgot things a whole lot more than normal. Now I’m
told that I have had a small stoke which is described as a small remote left thalamic lacunar infarct, sometime in the past but he can’t tell me when.
Medications: Lisinopril, Digoxin, Toprol, aspirin, Pravacol, Cholesterol: 180 Noral height & weight
After all that everyone keeps telling me I’m fine but I’m still tired all the time. My legs have been
sore the entire time I was in cardiac rehab, 24 sessions. I get lightheaded at different times
maybe 3 or 4 times a week lasting for a short time but nothing specific seems to cause it.
And a host of other things from forgetfulness to angina.
Question 1: What is the stuff about hypokenisis, perfusion defect, ejection fraction, and pulmonary hypertension.
Question 2: They say they can’t tell me when the stoke occurred but that it is older. Is older like 4 months or maybe a year or 10 years. Is there any way to tell?
Question 3: Should I be worried even though doctors seem to think I am fine. I’ve been
In the hospital 3 times in a year and a half and never before that.
Ischemic cardiomyopathy, CAD, MI, Cardiac arrest; inductable vtach, chronic angina, atrial fib, ventricular fib, dislipidemia, syncope, sick sinus syndrome, severe hypokinesis of the anterior wall, anterior septal wall, and the left ventricular apex. Also a marked anterior, septal, and apical perfusion defect with absent tracer uptake extending form the basil to the distal left ventricular segments which revealed no evidence of redistribution on the delayed images.
LVEF of between 20% and 35% according to which test and when. Pulmonary artery systolic pressure estimated at 44 mmHg consistent with pulmonary hypertension.
8/26/03 I was told after MI that I only had a 10% plaque in my arteries and nothing was done until it reached at least 50%.
01/18/04 Second MI was called acute with total blockage of one of the arteries. Reports also say I was in cardiogenic shock. Have a large scar on my anterior wall. EF 18-22%.
3/30/05 Third and fourth attacks were more like passing out. The first of these I didn’t tell anyone and the second my wife found me approximately 15 minutes after it started and thought I was having a seizure along with a heart attack. Anyway, back to the hospital and I am told I have ventricular fib, ventricular tycardia, sick sinus syndrome, and syncope and they put in a defibulator. EF 30-36%
7/26/05 Had another stress test done. Poor heart rate recovery, 1mm upsloping ST segment depression, lv dialated with evidence of severe hypokinesis to akinesis of the anterior wall, interventricular septum, distal inferior wall, distal lateral wall, and left ventricular apex. EF 25%
7/26/05Then I go to my regular doctor later to get a shoulder problem looked at and my wife made him give me a ct scan because I forgot things a whole lot more than normal. Now I’m
told that I have had a small stoke which is described as a small remote left thalamic lacunar infarct, sometime in the past but he can’t tell me when.
Medications: Lisinopril, Digoxin, Toprol, aspirin, Pravacol, Cholesterol: 180 Noral height & weight
After all that everyone keeps telling me I’m fine but I’m still tired all the time. My legs have been
sore the entire time I was in cardiac rehab, 24 sessions. I get lightheaded at different times
maybe 3 or 4 times a week lasting for a short time but nothing specific seems to cause it.
And a host of other things from forgetfulness to angina.
Question 1: What is the stuff about hypokenisis, perfusion defect, ejection fraction, and pulmonary hypertension.
Question 2: They say they can’t tell me when the stoke occurred but that it is older. Is older like 4 months or maybe a year or 10 years. Is there any way to tell?
Question 3: Should I be worried even though doctors seem to think I am fine. I’ve been
In the hospital 3 times in a year and a half and never before that.
Doctor's Answer
by CCF-M.D.-MJM, Aug 07, 2005 12:00AM
Hi dwolfe,
Question 1: What is the stuff about hypokenisis, perfusion defect, ejection fraction, and pulmonary hypertension.
The hypokinesis is an area of damaged heart muscle that still contracts versus akinesis which is an area of heart muscle that doesn't contract at all. The perfusion defect they describe is scar -- dead myocardium from your heart attack. Ejection fraction can vary depending on the type of study and inter reader variability. You have a moderate to severe reduction in your ejection fraction -- that is the take h ome message. You have mild pulmonary hypertenion, most likely caused by your LV dysfunction and heart failure.
Question 2: They say they can’t tell me when the stoke occurred but that it is older. Is older like 4 months or maybe a year or 10 years. Is there any way to tell?
There is no easy way to tell.
Question 3: Should I be worried even though doctors seem to think I am fine. I’ve been
In the hospital 3 times in a year and a half and never before that.
I think you should do your best to maintain a low salt diet, eat healthy and take your medications. I agree with all your medications but would consider changing pravacol to atorvastatin (lipator) because I think it is slightly a better medication. You also could consider a aldosterone blocker like spironolactone.
Otherwise it sounds like they are doing the right things. I hope this helps -- good luck.
Question 1: What is the stuff about hypokenisis, perfusion defect, ejection fraction, and pulmonary hypertension.
The hypokinesis is an area of damaged heart muscle that still contracts versus akinesis which is an area of heart muscle that doesn't contract at all. The perfusion defect they describe is scar -- dead myocardium from your heart attack. Ejection fraction can vary depending on the type of study and inter reader variability. You have a moderate to severe reduction in your ejection fraction -- that is the take h ome message. You have mild pulmonary hypertenion, most likely caused by your LV dysfunction and heart failure.
Question 2: They say they can’t tell me when the stoke occurred but that it is older. Is older like 4 months or maybe a year or 10 years. Is there any way to tell?
There is no easy way to tell.
Question 3: Should I be worried even though doctors seem to think I am fine. I’ve been
In the hospital 3 times in a year and a half and never before that.
I think you should do your best to maintain a low salt diet, eat healthy and take your medications. I agree with all your medications but would consider changing pravacol to atorvastatin (lipator) because I think it is slightly a better medication. You also could consider a aldosterone blocker like spironolactone.
Otherwise it sounds like they are doing the right things. I hope this helps -- good luck.
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defibrillator for cardiomyopathy (11 replies):I entered the CCF in 1992 with ideopathic dilated cardio...[more]
Chronic heart failure is associated with an increase in both atrial and ventricular arrhythmias. Carvedilol has a demonstrated antiarrhythmic effect, especially in patients with ischemic cardiomyopathy, which may result from several different
electrophysiological mechanisms. Adrenergic receptor blockade itself is well recognized to reduce myocardial ischemia and to improve arrhythmic thresholds. In addition, carvedilol possesses membrane-stabilizing characteristics, as well as the
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Carvedilol, long-acting metoprolol succinate, and bisoprolol (used only in Europe) have all been found effective for the treatment of patients with heart failure due to LV systolic
dysfunction. Large, randomized, placebo-controlled clinical trials with metoprolol succinate (Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure [MERITHF]),
bisoprolol (Cardiac Insufficiency Bisoprolol Study [CIBIS]-II), and carvedilol (U. S. Carvedilol Heart Failure Study)have all shown a significant reduction in all-cause mortality in heart failure patients. Although the MERIT-HF and CIBISII trials included some patients with New York Heart Association (NYHA) class IV heart failure, carvedilol is the only ß-blocker shown to reduce mortality in a large, randomized, placebo-controlled trial involving only patients with severe, advanced heart failure. It has been suggested that the more complete adrenergic blockade produced by carvedilol as well as its ancillary properties might confer a greater survival benefit than seen with 1-selective agents. In order to test the relative effects of carvedilol and metoprolol on clinical outcomes, the Carvedilol or Metoprolol European Trial (COMET)
randomized 3000 heart failure patients to treatment with either
carvedilol or short-acting metoprolol at comparable ß-blocking doses. The long-acting metoprolol succinate used in the MERIT-HF trial had not yet become available for use during this trial. In this head-to-head trial, carvedilol treatment was associated with a nearly 20% survival advantage compared to metoprolol over a 5-year period.1 CIBIS-II results associated bisoprolol with a greater rate of stroke than placebo. Equivalent average heart rates after 16 months indicated that the actual carvedilol and metoprolol doses used in COMET achieved comparable ß-blockade. However, the formulation and dosage of metoprolol used in COMET have been the subject of
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Carvedilol in Clinical Trials Carvedilol in Patients With Severe Heart Failure: The COPERNICUS Trial
The morbidity and mortality benefits of carvedilol in severe heart failure were investigated in the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial. This large, multicenter, double-blind trial randomized 2289 patients with heart failure symptoms at rest or minimal exertion (NYHA class IV) and a left ventricular ejection fraction (LVEF) less than 25% to treatment with carvedilol or placebo. Patients were
required to be clinically euvolemic on stable doses of ACE inhibitors and diuretics. The study was stopped early because carvedilol conferred a statistically significant survival benefit that exceeded the predefined stopping criteria set by the study’s data and safety monitoring board. Compared to placebo, patients receiving carvedilol had a 35% reduction of risk of death after a mean follow-up of 10.4 months. There was also a 24% reduction in the combined rate of all-cause death
or hospitalization, and a 27% reduction in the combined rate of cardiovascular death or hospitalization. In a subgroup of patients at particularly high risk of cardiac events, carvedilol treatment provided a 39% reduction in the risk of death and a 29% reduction in the rate of death or hospitalization, when compared to placebo.55 These findings are particularly important since they negate the long-standing impression that heart failure patients at high risk respond poorly to ß-blockade. Moreover, the benefit obtained during
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Although the benefit of ß-blocker therapy on mortality rates after MI was established in the early 1980s, clinical trials demonstrating this benefit had generally excluded patients
with significant heart failure, and ß-blocker use has specifically been avoided in these patients due to the
fear of precipitating pulmonary edema or cardiogenic shock following the withdrawal of sympathetic support. Since then, ß-blocker use has become further marginalized by the emergence of other mortality-reducing treatments including thrombolysis, angioplasty, and ACE inhibitor, intravenous-nitrate, aspirin,
heparin, and statin therapies. However, significant survival benefits from ß-blocker use in patients with heart failure, such as ischemic cardiomyopathy and prior MI, have renewed interest in ß-blocker therapy for post-MI patients with LV
impairment.
CAPRICORN (Carvedilol Post- Infarct Survival Control in LV
Dysfunction) was the first clinical trial specifically designed to study post-MI patients with confirmed LV systolic dysfunction, with or without clinical heart failure, and the
only large-scale post-MI ß-blocker trial performed in the modern, postthrombolytic era. The trial randomized nearly 2000 acute MI patients with an ejection fraction less than 40% to carvedilol or placebo; patients were also required to receive an ACE inhibitor for at least 48 hours. Nearly half underwent thrombolytic therapy or angioplasty and the majority was treated with aspirin, heparin, and nitrates. Only 10% received
immediate intravenous ß-blockers. Carvedilol reduced all-cause mortality by 23%, similar to earlier ß-blocker trials that did not include heart failure patients. Carvedilol treatment was also associated with a significantly lower incidence of cardiovascular mortality (25%), recurrent nonfatal MI (41%), and the combined end point of death or reinfarction (29%) (Figure 5). Both atrial and ventricular arrhythmias occurred significantly less frequently in patients randomized to carvedilol than to placebo (52% and 63%, respectively). However, there were no significant differences from placebo in
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Sorry it was sooooooo long but maybe it helped... Good Luck and keep us informed!
Eucardic is also another name for carvedilol,apparently the drug of choice for MOST patients with CHF.
http://bmj.bmjjournals.com/contents-by-date.0.shtml
http://www.clinicalcardiology.org/previous.html
http://heart.bmjjournals.com/contents-by-date.0.shtml
http://circ.ahajournals.org/contents-by-date.0.shtml
http://www.freemedicaljournals.com/
Good luck in your quest for information... Sorry if I didn't provide an answer you were looking for but as I mentioned before, I am only a second year medical student...