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Heart attack...

May 18, 2013 - 0 comments

maybe maybe not? I know how quirky EKG/ECG machines are so I'm really hoping this time it's a false reading.

My Primary found a new murmur and I've been so sick for about 5-6 months; not feeling right, more winded than normal, major headaches, different types of chest pain than before and ALOT more fainting spells even with my ICD.  

Cardiologist looked over my history and symptoms did an EKG and it shows Can't rule out Anterior MI; age unknown - I had my last EKG 9/28/2012 so they can narrow it down if it that's what it was.

My May 2013 EKG:
http://www.medhelp.org/user_photos/show/420033?personal_page_id=861727

Vent Rate:         64  
PR                    152
QRSD               94
QT/QTc             410/419  
P/QRS/T Axes   23/29/26

Sinus Rhythm
Cannot rule out Anterior Myocardial Infarction, age undetermined (V4)
Low QRS Voltage in Chest leads
*abnormal ecg*

finally

Sep 20, 2012 - 0 comments

after another episodes of blackouts; I can sit up without intense pain and my left arm/wrist is feeling better but still numb and all tingly...glad I didn't break anything this time...when will these blackouts end?

HCM/HOCM

Aug 14, 2012 - 0 comments

Hypertrophic Cardiomyopathy (idiopathic hypertrophic subaortic stenosis (IHSS) or asymmetrical septal hypertrophy (ASH)

http://emedicine.medscape.com/article/152913-overview

The overall prevalence of HCM is low and has been estimated to occur in 0.05-0.2% of the population. HCM is slightly more common in males than in females; presents at a younger age in females and females tend to be more symptomatic and are more likely to be disabled by their symptoms than males.  The most common presentation is in the third decade of life, but it may present in persons of any age, from newborns to elderly individuals; with the vast majority of cases occurring in the age range between the third and sixth decades of life.

The disorder has a variable presentation and carries a high incidence of sudden death. In fact, HCM is the leading cause of sudden cardiac death in preadolescent and adolescent children. The hallmark of the disorder is myocardial hypertrophy that is inappropriate, often asymmetrical, and occurs in the absence of an obvious inciting hypertrophy stimulus. This hypertrophy can occur in any region of the left ventricle but frequently involves the interventricular septum, which results in an obstruction of flow through the left ventricular (LV) outflow tract.

HCM can be separated into obstructive and nonobstructive types. Obstructive HCM is due to midsystolic obstruction of flow through the LV outflow tract as a result of a Bernoulli effect–induced systolic anterior mitral valve movement toward the septum.

HCM is a familial disease. There are defects in several of the genes encoding for the sarcomeric proteins, such as myosin heavy chain, actin, tropomyosin, and titin.

The significance of this obstruction, however, is highly controversial. Some investigators and experts believe the obstruction has less to do with the overall hemodynamic and pathophysiologic manifestations of this entity than it does with the inappropriate segmental hypertrophy, which, with its increased myocardial oxygen consumption and substrate for fatal ventricular arrhythmias, has much more significance in the overall clinical picture of this entity and in the treatment and prognosis of HCM.

Patients with some mutations, such as specific tropomyosin substitutions, have only a mild degree of ventricular hypertrophy, with little or no LV outflow tract obstruction, but they still carry a disproportionately high risk for sudden death.


Complications of HCM may include the following:

•Congestive heart failure
•Ventricular and supraventricular arrhythmias•
•Infective mitral endocarditis
•Atrial fibrillation with mural thrombus formation
•Sudden death

Most patients with HCM have abnormal diastolic function (whether or not a pressure gradient is present), which impairs ventricular filling and increases filling pressure, despite a normal or small ventricular cavity. These patients have abnormal calcium kinetics and subendocardial ischemia, which are related to the profound hypertrophy and myopathic process.

Reported annual mortality rates in patients with hypertrophic cardiomyopathy (HCM) have ranged from less than 1% to 3-6%, and studies suggest that they have significantly improved over the past 40 years.[11]

A 2006 study reported that published sudden death rates over the previous 10 years were lower than were previously published figures (median 1.0% (range 0.1–1.7) v 2.0% (0–3.5)). Nevertheless, HCM still carries a high risk for mortality and morbidity

Most patients with HCM are asymptomatic. Unfortunately, the first clinical manifestation of the disease in such individuals may be sudden death, likely from ventricular tachycardia or fibrillation. Younger patients, particularly children, have a much higher mortality rate.

Patients can have a myriad of arrhythmias, including atrial fibrillation, atrial flutter, ventricular ectopy, ventricular tachycardia, and ventricular fibrillation. These patients are among the highest-risk group for ventricular fibrillation and pose difficult therapeutic decisions for risk reduction.

Patients have a high likelihood of recurrent heart failure resulting from mitral regurgitation and profound diastolic dysfunction. HCM is a progressive condition that worsens over time, as does the gradient across the LV outflow tract if left untreated. Systolic function usually is well preserved until the late stages of the disease. Angina is rare in children but common in adults. Syncope and presyncope are common and may identify individuals at high risk for sudden death.

In more than 80% of cases, the arrhythmia that causes sudden death is ventricular fibrillation. Many of these cases degenerate into ventricular fibrillation from rapid atrial arrhythmias, such as fibrillation, supraventricular tachycardia, or Wolff-Parkinson-White syndrome, while others result from ventricular tachycardia and low cardiac output hemodynamic collapse.

Common electrocardiographic findings include ST-T wave abnormalities and LV hypertrophy. Other findings observed on ECG include axis deviation (right or left), conduction abnormalities (P-R prolongation, bundle-branch block), sinus bradycardia with ectopic atrial rhythm, and atrial enlargement. One mutation has been identified that is associated with hypertrophic cardiomyopathy (HCM) and Wolff-Parkinson-White syndrome.

Uncommon findings include an abnormal and prominent Q wave in the anterior precordial and lateral limb leads, short P-R interval with QRS suggestive of preexcitation, atrial fibrillation (poor prognostic sign), and a P-wave abnormality, including left atrial enlargement.

Findings on Holter monitoring and event electrocardiography commonly include atrial and ventricular ectopy, sinus pauses, wandering atrial pacemaker, atrial tachycardia, atrial fibrillation and/or flutter, and nonsustained ventricular tachycardia.

Beta-Adrenergic Blocking Agents reduce the inotropic state of the left ventricle. They decrease diastolic dysfunction and increase LV compliance, thereby reducing the pressure gradient across LV outflow tract. Beta-adrenergic blocking agents decrease heart rate, thus lowering myocardial oxygen consumption and reducing the potential for myocardial ischemia.

Propranolol (Inderal LA, InnoPran XL) Propranolol is a class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases the automaticity of contractions. The dose is titrated to a heart rate of between 50 and 60 bpm.




My Personal Heart Page

Sep 26, 2011 - 0 comments

Diagnosis, surgery and test results

PVC's - frequent (50,000); malignant pvc's
VT/Vtach - Polymorphic Ventricular Tachycardia
HOCM (obstructed Hypertrophic Cardiomyopathy)
Recurring Syncope (fainting) since age 9
Dysautonomia (autonomic dysfunction)
Neurocardiogenic Syncope
Orthostatic Intolerance
PAC's
PSVT
Moderate Obstructive Sleep Apnea
Non-Ischemic Cardiomyopathy
Pacemaker/ICD (defibrillator) Teligen 100
Autonomic Nervous System Dysfunction
Hypothyroidism
Bipolar & Depression
PTSD
Anxiety disorder w/agoraphobia
Endometriosis
Adenomyosis
Degenerative Disc Disease (auto accident in 1999)
Radiculopathy
Arthritis & Bone spurs on the front and back of my spine
L3, 4 & 5 Bulging & Herniated Discs
Sacroiliitis
Low Back Pain Syndrome

Test & Surgery Results -

[EKG's]
Check http://www.medhelp.org/user_photos/list/967168?personal_page_id=861727 for my ekg's and ICD info.
4/27/2007 EKG
Vent Rate:         51  
PR                   142
QRSD               110
QT/QTc             380/350  
P/QRS/T Axes   58/80/63
Interpretation: Multiple PVC's; Short RR Wide QRS; Incomplete RBBB; QT Interval too short for rate

11/21/2008 (3rd EKG in a row, did not get other results)
RR                   1018
PR                     150
QRSD                100
QT/QTc              420/417
QT disp               58
P/QRS/T Axes    12/53/22
Normal ECG except for rate [Sinus Bradycardia] vent rate 58


6/25/2009 EKG
Vent Rate:         74  
PR                    136
QRSD               108
QT/QTc             402/426  
P/QRS/T Axes   63/59/34
Interpretation: Sinus Rhythm with PVC's; NonSpecific Septal T Wave Changes


6/25/2009 EKG
Vent Rate:         80  
PR                    146
QRSD               110
QT/QTc             404/439  
P/QRS/T Axes   63/59/34
Interpretation: Sinus Rhythm with frequent PVC's; Poor R Wave progression; NonSpecific Septal T Wave Changes


7/14/2009 EKG
Vent Rate:         78  
PR                   154
QRSD               106
QT/QTc             384/437  
P/QRS/T Axes   81/84/68


7/26/2009  EKG
Vent Rate:         85  
PR                   146
QRSD               102
QT/QTc             398/473  
P/QRS/T Axes   61/56/36
Interpretation: Frequent PVC's; Low voltage QRS; Prolonged QT; Multifocal PVC's


8/26/2009     EKG
Vent Rate:         54
PR Interval         152
QRSD                98  
QT/QTc             434/411  
P/QRS/T Axes   70/74/43
notes: Low Voltage QRS; Sinus Bradycardia with sinus arrhythmia


8/27/2009     EKG
Vent Rate:         60
PR Interval         164
QRSD                98  
QT/QTc             434/434  
P/QRS/T Axes   30/56/19  
notes: Low Voltage QRS


8/28/2009     EKG
Vent Rate:         60
PR Interval         134
QRSD                96  
QT/QTc             430/430  
P/QRS/T Axes   56/70/42
notes: Electronic Atrial Pacemaker; Low Voltage QRS;  borderline ECG when compared with ECG of 8/27/2009 electronic atrial pacemaker has replaced sinus ryhthm.


1/15/2010     EKG
Vent Rate:       77
PR Interval      142
QRSD               110
QT/QTc             380/410  
P/QRS/T Axes   26/61/26  
RSR (V1)
Result: Probably normal


2/4/2011 EKG
Vent Rate:          81
PR Interval          134
QRSD                106  
QT/QTc              374/411
P/QRS/T Axes   26/58/25


7/8/2011 EKG (Abnormal)
Rate 65 bpm
PR 164
QT/QTc  410/418
QRSD 106
P Axis 34
QRS Axis 45
T Axis 26
Interpretation:  Sinus Rhythm;  Low Voltage QRS in precordial Leads; -RSR (V1)

May 2013 EKG:
http://www.medhelp.org/user_photos/show/420033?personal_page_id=861727

Vent Rate:         64  
PR                    152
QRSD               94
QT/QTc             410/419  
P/QRS/T Axes   23/29/26

Sinus Rhythm
Cannot rule out Anterior Myocardial Infarction, age undetermined (V4)
Low QRS Voltage in Chest leads


  
[Cardiac Tests]

7/1/2009 24 hr holter results:
Roughly 50,000 PVC's in a 24 hr period.
The predominant rhythm is sinus with ventricular bigeminy and trigeminy and an average rate of 89 beats per minute.  
Minimum heart rate of 67 and a maximum heart rate of 131 beats per minute.  
The longest run was 3 beats long and the fastest run was at 170 beats per minute at 15:51 and 5:44 respectively.  
2 premature atrial contractions in 24 hours
very frequent complex ventricular ectopys with bigeminy & trigeminy.
2 runs of NSVT, 2 couplets, 3 triplets, 2 atrial contractions
Rare atrial ectopy


7/6/2009 Stress test:  4:55 min test
Resting - Sinus rhythm with slow R wave progression in the precordial leads
Stress - Frequent pvc's w/ 2 PVC couplets and 1 PVC triplet in recovery [1 min]
Sinus Tachycardia with no signifiant ST-T wave changes
QRS segment of PVC's narrowed substantially with exercise, widening again in recovery (180 ms to 80 ms)
BP - 130/70 - 150/90

Heart rate response: resting 74 bpm, peak 154 bpm, 87% age predicted maximum. 1 min into recovery heart rate decreased to 121 bpm
Functional aerobic impairment of 35% 6 mETS achieved
Increasing Dyspnea was noted with exercise stress as well as increasing dizziness.  Nausea was noted in recovery and I fainted


7/26/2009 - ER report says suspicous CP & CHF symptoms.


8/26/2009 Tilt table test
BP 126/79 HR 77 - Start
BP 129/87 HR 101 - 20 min
BP 137/71 HR 109 Nitroglycerin given
By minute #4 after Nitro was given, the patient had a syncopal event with no palpable pulse
BP 97/48 HR 78 - supine state

Findings: Profound Sinus Bradycardia; Classic symptoms of neurocardiogenic syncope with cardioinhibitory and vasodepressor responses (NCS & OI)


8/26/2009 RF Ablation
Part #1 http://www.medhelp.org/user_photos/show/206123?personal_page_id=861727
Part #2 http://www.medhelp.org/user_photos/show/206124
Part #3 http://www.medhelp.org/user_photos/show/206125

8/26/2009  RF Ablation (I condensed it)

Ventricular pacing protocol was performed and consisted of decremental ventricular pacing and ventricular programmed stimulation with 1 pacing drive cycle length and up to 3 extra stimuli delivered from the RV apex, and at this point with double extra stimuli, the patient was induced into polymorphic ventricular tachycardia, which became sustained and required a 360-joule counter shock back to sinus rhythm.

This was reproducible but non sustained with double and reproducible nearly sustained with triple all at baseline.

Long runs of  polymorphic ventricular tachycardia were reproduced, and with triple extra stimuli, a long sustained run was induced, which terminated just before external defibrillator discharge.

The patient continued with ventricular bigeminy.  The pvc's were that of a left bundle inferior axis with a notched QRS complex across the precordial leads in a transition between V3 & V4, consistent with a right ventricular free wall outflow tract site.  It was also positive in both lead V1 and aVL consistent again with a more posterior site within the RV outflow tract.

The PVC's were mapped to a location that existed in the posterior to free wall area of the RVOT.   A superior site was noted with highly fractioned signals very early compared to the onset of the QRS and 135 msec earlier than the reference surface lead.

The longest sinus node recovery time was 808 msec with the longest corrected sinus node time of 203 msec

Post procedure ECG demonstrated NSR and nonspecific T wave abnormality.

dx: Malignant ventricular arrhythmia's w/sudden cardiac death


8/27/2009 Cardiac MRI
LV Mass – [Average: 141 grams] 105g
LV End Diastolic Volume – [Females 20-50 - Average: 118 ml] 100ml
LV End Systolic Volume – [Females 20-50 - Average: 42ml] 30.5ml
Normal LV Wall Thickness - [10mm] 11 on echo; 12 on MRI
Cardiac Output - 4.9 liters/min
Stroke Index - 28.89
Cardiac Index - 2022
LV (5.1cm) and RV (3.7cm) end diastolic midchambers  
RV end diastolic midchamber lateral wall (4mm)

No evidence points to ARVD, LV is limited due to wall motion degredation and patient movement since I couldn't complete the test - inconclusive results - further testing needed


8/28/2009 Cardiac Catherization
Hemodynamic assessments demonstrates mild systemic hypertension and moderately elevated LVEDP.
The coronary circulation is co-dominant.  There was no angiographic evidence for CAD.
EF: 40%
Aortic Pressure (S/D/M) 120/70/90
Left Ventricle (s/edp) 120/34
dx: Non-Ischemic Cardiomyopathy with an ejection fraction of 40%; no kinks, plaque, blocks or clots


[Echocardiograms]

7/6/2009 Echocardiogram (Abnormal)
LVEDD      44 [35-57]
LVESD      36 [23 - 40]
Left atrium 39 [19-40]
LVIS         12  [6-11]
LV posterior wall 11 [6-11]
Ascending Aorta 29 [21 - 34]

Interpretation:
Mild Tricuspid insufficency
Trace Mitral valve in sufficency
Pulmonic valve was not well visualized due to a technically difficult 2D echo
Mild Concentric left ventricular hypertropy  with EF rate of 55 - 60%
Dilated left atrium with normal left atrial pressures
LV diastolic function: E/A 1.0, DT a140 msec, E' 10/cm/sec E/E' 8


3/17/2011 Echocardiogram -  Abnormal (notes: this is a technically difficult study)
LVEDD       46.2mm [35-56]
LVESD       27.4 mm [22-43]
Left atrium  30.5 mm [19-40]
LVIS          12.3  [8-12]
LV posterior wall 12.5 mm [8-12]
Aortic Root 31.2 mm [26-36]
EF 71%
Aortic Valve Velocity 1.30m/s

Interpretation:
Left Ventricular Hypertrophy
Mitral valve regurgitation
Tricuspid valve regurgitation with a peak velocity of 1.76 m/s w/peak gradient of 12.3 mmHG
Estimated PA pressure is 22.3 mmHG


9/1/2011 Echocardiogram
LVEDD       48mm [35-56]
LVESD       31 mm [25-41]
Left atrium   41 mm [19-40]
LVIS           12.0   [8-11]
LV posterior wall 12.0 mm [8-11]
Aortic Root  32 mm [26-36]
EF 60%
LA Pressure 16.43mmHg
LA Volume 63mL
LAVI 25mL/m2
RV systolic pressure is 29 mmHG
LV Mass 87
E Velocity 93
E/A Ratio 1.35 [>1]
E/e ratio 11.62
PHT 67msec <90
DT 230msec [160-240]

Impressions:
Left Ventricular Hypertrophy
Dilated Left Atrium
Tricuspid valve regurgitation - Right atrial pressure is 5mmHg.  Tricuspid velocity 247cm/s.
Pulmonic Valve regurgitation