LV global wall hypokinesis

[ramlin]

I recently had a Nuclear Stress Test which revealed severe abnormalities with a large
septal apical inferior defect with mild reversibility on perfusion images. (What does mild
reversiblity mean in the context used here?)

The left ventricle was severely globally hypokinetic with more prominent septal wall
hypokinesis with EF of only 24%. (What does this mean in layman's terms?)

Echocardiogram matched the nuclear strudy, and the  EF was only 15-20%.
There is mild left ventricular enlargement, mild left atrial enlargement, diastolic
dysfunction, and aortic sclerosis. (Here again what does this mean in layman's
terms?)

Finally, what are the procedures for treating the above conditions?

Thank you
Marlin in Florida

[kenkeith]

i AM TRYING TO UNDESTAND MY ECHO CARDIOGRAM REPORT,
CAN ANY BODY EXPLAIN WHAT IS

-ANTEROAPCIAL HYPOKINESIS.  
Hypokinesis is heart wall movement impairment at location (anteroapical).

-DIASTOLIC IMPAIRMENT ESPECIALLY ON VALSALVA
The heart is monitored by ECG, pressure recording, or other methods while the patient performs the Valsalva maneuver; carciac volume decreases in unaffected patients but may dilate in the patient with impaired myocardial reserve.  Diastolic impairment is an abnormality during the filling phase of the heart beat.

-TR 1 DEGREE
The  clinical grade (0, 1+, 2+, 3+, and 4+) indicate the severity of tricuspid valve.  Tricuspid valve is to provide one-way passage of blood flow from the left ventricle to circulatory system.  TR 1 DEGREE indicates some blood is leaking back into the LV.

-PA L 25 MMHG
Pulmonary hypertension is defined as a mean PA pressure greater than 25 mm Hg.




Continuous Doppler measurements were taken in the left ventricular outflow tract at the level of the aortic valve. Cardiac output was calculated by multiplying the velocity-time integral by aortic valve area and heart rate. Simultaneous pulmonary artery catheter measurements were taken averaging the results of the three 10-cc boluses of iced saline. The difference between the methods was 0.5+/-1.1 l/min (mean +/-2 SD) in patients with no or 1st degree TR (r=0.96), 0.8+/-2.0 l/min in those with 2nd degree TR (r=0.92), and 1.9+/-2.3 l/min in those with 3rd degree TR (r=0.69). CONCLUSIONS: A high degree of TR is associated with underestimation of cardiac output measured by thermodilution.
Objective: To determine the relationship between the degree of tricuspid regurgitation (TR) and accuracy of cardiac output measurement by thermodilution in mechanically ventilated patients. Design and setting: Prospective observational study in a 20-bed general intensive care unit in the university hospital. Patients: We examined 27 patients (not undergoing cardiac surgery): 8 with no or 1st degree TR, 9 with 2nd degree, and 10 with 3rd degree TR. Interventions:
and pulmonary vascular resistance of >120 dynes?sec–1?cm–5. HPS was defined as postural hypoxemia with a positive contrast echocardiogram demonstrating intrapulmonary shunting in a patient with severe liver disease.

[suedihaider]

i AM TRYING TO UNDESTAND MY ECHO CARDIOGRAM REPORT,
CAN ANY BODY EXPLAIN WHAT IS
-ANTEROAPCIAL HYPOKINESIS

-DIASTOLIC IMPAIRMENT ESPECIALLY ON VALSALVA

-TR 1 DEGREE

-PA L 25 MMHG

[kenkeith]

The test was performed to analyze wall motion defect (hypokinesis) of the left ventricle (pumping chamber) and septum (wall between chambers).  The defect is/can be the result of a heart attack causing necrosis (death of cells) or ischemia (lack of blood flow to the heart tissues).  Sometimes with hypokinesis the cells are in hypernation or stunned and with treatment to increase blood supply to the deficit area the cells can recover.  Reversibility is the return to normal or near normal after a period of rest during the testing phase.

Global hypokinesis of the LV indicates symetrical enlargement and septum is thickened and less flexible.

The fraction of blood pumped into circulation with each heart beat is termed ejection fraction (EF).  Normal is an EF of 55 to 75%, and heart failure range is below 29%.  When the heart walls are thickened and the chamber dilated with damaged heart cells the contractions will be weak and EF will be low.

Diastolic dysfunction addresses the filling phase of the left ventricle.  If the walls are thickened, there will be less space for the filling phase and cardiac output will be reduced accordingly.  

Aortic sclerosis is the narrowing of the aortic valve (usually due to calcification with age) and the will adversely add pressure to the left ventricle and dilate left atrium and left ventricle.  The report indicates the condition is mild and I have outlined the worst case scenario.

About 4 years ago my EF was below 29%.  With medication my heart size is currently normal as well as an EF55%.  I had some hypokinesis at the distal portion of the heart.  A stent in a coronary artery increased blood flow and there is very little heart wall motion defect if any.

The medication is an ACE inhibitor that will dilate blood vessels and lightened the load the heart has to pump against.  Also a beta blocker and for a while a diuretic,  digoxin to strenghten contractions, aspirin.  And isosorbide for chest pains (angina) when needed.  Sometimes the heart will fully recover form a heart attack. Apparently, I had a silent heart attack as I had no indication until congested heart failure.