Pat
Risser (Patrick)
154
Ronald Ave.
Ashland,
OH 44805
(503)
655-2530 – home
(419)
908-9335 – cell
Emergency Contact:
Patricia Sandoval
(significant other)
Heart
Problem
I visited a cardiologist on Monday, January 7, 2008 and he said my
heart has suffered substantial and significant deterioration. He recommended a defibrillator implant
ASAP.
His lack of bedside manner and the callous way in which he
interacted with me and Trish really put us off. It felt like he had delivered an emotional gut punch and
issued me a death sentence.
We decided that the best thing was to gather more information and
be retested and obtain a second (and perhaps a third or fourth) opinion. I am in no pain or discomfort. The only symptom is feeling tired and
short of breath. Overall, my
spirits are good and I am pretty much doing everything I've ever done.
I had to see my primary care doc to get a referral to another
cardiologist for a second opinion.
I saw the cardiologist on Tuesday, January 22, 2008. He confirmed the diagnosis and
recommendation. I saw the cardiac
electrophysiologist who will do the surgery on Thursday, January 24, 2008.
The cardiologists said my heart is bad ("ejection fraction
15") to the point where I was high risk of sudden cardiac death. That's those folks you hear about who
are eating dinner and suddenly slump over dead or the guy who is watching TV
and just keels over dead or the woman who goes to sleep and never wakes up.
A bunch of years ago, sudden cardiac death episodes (ventricular
fibrillation) would kill 97%. Once
in a while, paramedics would show up, zap the person with the paddles and
restart their heart. Only 3%
survived and those were the candidates that got defibrillator implants. Eventually, heart docs got a clue and
started to think about what the risk factors were and started putting
defibrillators in those who might have an episode.
I'm one of those who might have an episode. Of those who get defibrillators, a year
later, 2 will not have needed it.
But, one will come in and shake the docs hand and say thanks for saving
my life. There's no way to predict
which one of the three I will be.
I might live the rest of my life and never have an episode. On the other hand, if an episode should
occur my chances of survival are very high with the implant.
I went into the hospital and had the surgery done on Monday,
January 28, 2008 at MedCentral Hospital in Mansfield. I went in the morning, had surgery in the afternoon and was
discharged on Tuesday around noon.
I went home to rest and recover.
It'll take a few days/weeks to heal but I'll have the comfort of the
"insurance" of knowing I'll likely survive if I have a future episode
of ventricular fibrillation.
I'm still a bit sore (a three-inch wound to put in a device the
size of a small deck of cards or a large pocket watch) from being sliced open
like cutting open a pork chop to stuff it. I can't drive for ten days and I'm not supposed to lift my
arm too high but I am healing slowly.
Actually, I think I'm probably healing quickly under the
circumstances. Modern medicine is
amazing. I tried to ask them to
take me back in next week for the rest of the bionics (both legs and my
pitching arm) but they didn't think my Medicare would cover it.
Thanks for caring.
Love,
Pat
Current
Heart History (most
recent first)
February 5,
2008
Follow-up
with Jon Benson, PA-C for removal of bandage
Mid-Ohio
Heart Clinic
680
Park Avenue West
Mansfield,
OH 44906
(419)
524-8151
January 29,
2008
Discharged
from MedCentral Hospital in Mansfield, Ohio hospital around noon
MedCentral
Hospital
335
Glessner Ave.
Mansfield,
OH 44903
419-526-8000
January 28,
2008
Monday,
11:00 a.m.
Went into
MedCentral Hospital in Mansfield, Ohio for surgical implant of
Medtronic
Virtuoso VR Defibrillator
Surgeon
was: Dr. Jeffery P. Courson, D.O.
Mid-Ohio
Heart Clinic
680
Park Avenue West
Mansfield,
OH 44906
(419)
524-8151
MedCentral
Hospital
335
Glessner Ave.
Mansfield,
OH 44903
419-526-8000
January 24,
2008
Thursday,
9:15 a.m.
See Cardiac Electrophysiologist
Dr.
Jeffery P. Courson, D.O.
Mid-Ohio
Heart Clinic
680
Park Avenue West
Mansfield,
OH 44906
(419)
524-8151
January 22,
2008
Tuesday,
10:00 a.m.
See
Cardiologist
Dr. Andrew
Fahmy
Samaritan
Medical Clinic Building
350
Hillcrest Drive
Ashland,
Ohio 44805
Main Office:
680 Park
Avenue West
Mansfield,
OH 44906
(419)
524-8151
Confirmed
diagnosis and strongly recommended defibrillator implant and made referral to
Cardiac Electrophysiologist, Jeffery P. Courson, D.O.
in the Mansfield office
January 18,
2008
Friday, 2:10
p.m.
See Primary
Care Physician
Dr. Stephen
Torski
2111
Claremont Ave.
Ashland, OH
44805
(419)
281-5575
Receeived
referral for 2nd opinion to cardiologist Dr. Andrew Fahmy
January 7,
2008
Monday, 3:30
p.m.
See
Cardiologist
Dr. Bruce
Fleishman, MD, FACC
At Samaritan
Hospital Ashland, OH
(419)
289-0491 x-3501
Said,
"heart has substantially and significantly deteriorated" and
recommended a Defibrillator implant
December 21,
2007
Friday,
11:30 a.m.
Samaritan
hospital for blood work and Echocardiogram
December 20,
2007
Thursday,
2:30 p.m.
See Primary
Care Physician
Dr. Stephen
Torski
2111
Claremont Ave.
Ashland, OH
44805
(419)
281-5575
Ordered blood
work, Echocardiogram and referral to cardiologist Bruce Fleishman
Medical/Family
History
Medical
History:
á
Born in
Ashland, Ohio September 24, 1952 at Samaritan Hospital
á
Tonsils
out 1954
á
First
three heart attacks,
Feb. 14, Mar. 7, Dec. 23, 1988 (Dr. Joseph Connelly, Denver, Colorado)
á
Fourth heart
attack October 13,
1994 (cardiologist: Dr. Jacque Chahin, Concord, California)
á
Fifth heart
attack January 27,
1997 (cardiologist: Dr. Mark Hattenhauer, Tualatin, Oregon) with stent implant;
Then
follow-up with Dr. William Davies, 19260 SW 65th
Ave., Pacific Heart Associates, Tualatin, OR 97062-5712. Phone, (503) 692-0405
á
Appendix
out July 22, 2006 (Samaritan Hospital) (while there, heart had atrial
tachycardia and diagnosis of ischemic cardiomyopathy)
Summary:
á
Serious
major needle phobia
á
No
major broken bones
á
No
known allergies
á
General health good
á
Started smoking age 7
á
Quit smoking December 2001 (age 49)
Family History:
á
Maternal grandfather died of heart attack age 60
á
Other
grandparents died old age
á
Mother generally healthy (born 10-30-32; age 75)
á
Father
(Eldred Risser) died in auto accident August 15, 1954
á
Maternal Aunt deceased around 1996 from apparent stroke
á
Maternal Uncle deceased September 30, 1999 suicide
á
Maternal Uncle with "heart problems" age 67
á
Brother Mike (one year younger; born 09-25-53) had stroke age 25,
stent implants for heart issues in his 40's and carotid cleared
á
Brother Rich (2 ½ year younger; born 04-30-55) claims he
takes nitro, is schizoaffective, is alcoholic
á
Daughter
Bridget born 1973 (healthy)
á
Daughter
Heather born 1975 (healthy)
á
Son
John born 1979 (healthy)
Background:
á
Moved
to Denver, Colorado 1960
á
Moved
to Mayfield Hts., Ohio 1968
á
Graduated
Mayfield HS 1970
á
Married
1972, moved to Colorado
á
Moved
to Cleveland 1973
á
Moved
to Colorado 1978
á
Graduated
Colorado College with BA, Philosophy 1983
á
Attended
Denver University Law School 1983-1985
á
Moved
to California 1990
á
Moved
to Oregon 1996
á
Moved to
Ashland, Ohio October 2005
Daily
Pills: (No Known Allergies)
Morning:
Lotensin
(Benazepril Hcl – 10 mg.)
Coreg
(25 mg.)
Lipitor
(10 mg.)
Furosemide
(Lasix – 20 mg.)
Folic
Acid (400 mcg.)
Multi-Vitamin
OneSource for adults 50+
B-12
(500 mcg.)
Glucosamine
Chondroitin Complex (1500 mg. and 1200 mg.)
Evening:
Lotensin
(Benazepril Hcl – 10 mg.)
Coreg
(12.5 mg.)
Allopurinol
(150 mg.)
Aspirin
(325 mg.)
Niacin
(time-released 500 mg.)
Vitamin
C (500 mg.)
Vitamin
E (400 I.U.)
Glucosamine
Chondroitin Complex (1500 mg. and 1200 mg.)
Background
for Heart info
This is my
primary diagnosis:
Ischemic cardiomyopathy
http://en.wikipedia.org/wiki/Cardiomyopathy
Ischemic
cardiomyopathy is a weakness in the muscle of the heart due to inadequate oxygen
delivery to the myocardium with coronary artery disease being the most common
cause. Anemia and sleep apnea are relatively common conditions that can
contribute to ischemic myocardium and hyperthyroidism can cause a 'relative'
ischemia secondary to high output heart failure. Individuals with ischemic
cardiomyopathy typically have a history of myocardial infarction (heart
attack), although longstanding ischemia can cause enough damage to the
myocardium to precipitate a clinically significant cardiomyopathy even in the
absence of myocardial infarction. In a typical presentation, the area of the
heart affected by a myocardial infarction will initially become necrotic as it
dies, and will then be replaced by scar tissue (fibrosis). This fibrotic tissue
is akinetic; it is no longer muscle and cannot contribute to the heart's
function as a pump. If the akinetic region of the heart is substantial enough,
the affected side of the heart (i.e. the left or right side) will go into
failure, and this failure is the functional result of an ischemic
cardiomyopathy.
Cardiomyopathy,
which literally means "heart muscle disease", is the deterioration of
the function of the myocardium (i.e., the actual heart muscle) for any reason.
People with cardiomyopathy are often at risk of arrhythmia or sudden cardiac
death or both. This is the reason
why my cardiologist has recommended:
Implantable Cardioverter-Defibrillator (ICD)
Also known as Automatic Internal Cardiac
Defibrillator (AICD). These devices are implants, similar to pacemakers (and
many can also perform the pacemaking function). They constantly monitor the
patient's heart rhythm, and automatically administer shocks for various life
threatening arrhythmias, according to the device's programming. Many modern
devices can distinguish between ventricular fibrillation, ventricular
tachycardia, and more benign arrhythmias like supraventricular tachycardia and
atrial fibrillation. Some devices may attempt overdrive pacing prior to
synchronised cardioversion. When the life threatening arrhythmia is ventricular
fibrillation, the device is programmed to proceed immediately to an
unsynchronized shock.
There
are cases where the patient's ICD may fire constantly or inappropriately This
is considered a medical emergency, as it depletes the device's battery life,
causes significant discomfort and anxiety to the patient, and in some cases may
actually trigger life threatening arrhythmias. Some emergency medical services
personnel are now equipped with a ring magnet to place over the device, which
effectively disables the shock function of the device while still allowing the
pacemaker to function (if the device is so equipped). If the device is shocking
frequently, but appropriately, EMS personnel may administer sedation.
An implantable cardioverter-defibrillator (ICD),
also known as an automated implantable
cardioverter-defibrillator (AICD), is a small battery-powered electrical
impulse generator which is implanted in patients who are at risk of sudden
cardiac death due to ventricular fibrillation. The device is programmed to
detect cardiac arrhythmia and correct it by delivering a jolt of electricity.
In current variants, the ability to revert ventricular fibrillation has been
extended to include both atrial and ventricular arrhythmias as well as the
ability to perform biventricular pacing in patients with congestive heart
failure or bradycardia.
The process of implantation of an ICD is similar
to implantation of a pacemaker. Similar to pacemakers, these devices typically
include electrode wire/s which pass through a vein to the right chambers of the
heart, usually being lodged in the apex of the right ventricle. The difference
is that pacemakers are more often temporary and generally designed to
consistently correct bradycardia, while AICDs are often permanent safeguards
against sudden abnormalities.
ICDs constantly monitor the rate and rhythm of
the heart and can deliver therapies, by way of an electrical shock, when the
electrical manifestions of the heart activity exceeds the preset number. More
modern devices can distinguish between ventricular fibrillation and ventricular
tachycardia (VT), and may try to pace the heart faster than its intrinsic rate
in the case of VT, to try to break the tachycardia before it progresses to ventricular
fibrillation. This is known as fast-pacing, overdrive pacing, or
anti-tachycardia pacing (ATP). ATP is only effective if the underlying rhythm
is ventricular tachycardia, and is never effective if the rhythm is ventricular
fibrillation.
Many modern ICDs use a combination of various
methods to determine if a fast rhythm is normal, ventricular tachycardia, or
ventricular fibrillation.
Rate discrimination evaluates the rate of the
lower chambers of the heart (the ventricles) and compares it to the rate in the
upper chambers of the heart (the atria). If the rate in the atria is faster
than or equal to the rate in the ventricles, then the rhythm is most likely not
ventricular in origin, and is usually more benign. If this is the case, the ICD
does not provide any therapy.
Rhythm discrimination will see how regular a
ventricular tachycardia is. Generally, ventricular tachycardia is regular. If
the rhythm is irregular, it is usually due to conduction of an irregular rhythm
that originates in the atria, such as atrial fibrillation.
Morphology
discrimination checks the morphology of every ventricular beat and compares it
to what the ICD believes is a normally conducted ventricular impulse for the
patient. This normal ventricular impulse is often an average of a multiple of
beats of the patient taken in the recent past.
In
July 2006 when I had my appendix out, my heart showed Atrial fibrillation.
Atrial fibrillation (AF or afib) is a cardiac
arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria)
of the heart. It is defined as being irregularly irregular, and can often be
identified as such when taking a pulse. Atrial fibrillation is the most common
arrhythmia; risk increases with age, with 8% of people over 80 having AF. In
atrial fibrillation, the electrical impulses that are normally generated by the
sinoatrial node are replaced by disorganized activity in the atria, leading to
irregular conduction of impulses to the ventricles that generate the heartbeat.
The result is an irregular heartbeat. This may be continuous (persistent or
permanent AF) or alternating between periods of a normal heart rhythm
(paroxysmal AF). The natural tendency of atrial fibrillation is to become a
chronic condition. Chronic AF leads to an increased risk of death.
Atrial fibrillation is often asymptomatic, and
is not in itself generally life-threatening, but may result in palpitations,
fainting, chest pain, or congestive heart failure. Patients with atrial
fibrillation are at significantly increased chance of stroke (about 2 to 7
times the regular population), and AF is a leading cause of stroke.
Atrial
fibrillation may be treated with medications which either slow the heart rate
or revert the heart rhythm back to normal. Synchronized electrical
cardioversion may also be used to convert AF to a normal heart rhythm. Surgical
and catheter-based therapies may also be used to prevent recurrence of atrial
fibrillation in certain individuals. People with AF are often given anticoagulants
such as warfarin to protect them from stroke.
In
cardiovascular physiology, ejection fraction (Ef) is the fraction of blood
pumped out of a ventricle with each heart beat. Normal is between 55 and 70. My ejection fraction is 15.
Damage
to the muscle of the heart (myocardium), such as that sustained during
myocardial infarction or in cardiomyopathy, impairs the heart's ability to
eject blood and therefore reduces ejection fraction. This reduction in the
ejection fraction can manifest itself clinically as heart failure. The ejection
fraction is one of the most important predictors of prognosis; those with
significantly reduced ejection fractions typically have a poorer prognoses.