The Conclusion from Medical Updates Part 1, Part 2, Part 2.5,
Part 3: The Cardiac MRI, & Part 3: The Exercise Stress Test
Although preparing for any type of doctors appointment is stressful enough for almost anyone, it is even harder when you have a chronic illness, or even worse – multiple chronic conditions.
There is always so much preparation and pressure that goes into getting ready for each appointment:
However, it’s entirely worse when you know you are awaiting abnormal tests results.
My list of questions for my cardiologist had gotten so long,
I was afraid to even present it to the cardiologist:
- Medication questions:
- Should I take the beta-blockers in the morning or evening?
- Will I stay at this dose?
- Abnormal test result questions:
- Could this condition be genetic? Is it associated to a particular gene or chromosome?
- Could the cardiac issues be caused by the vascular compressions or vice-versa?
- Could I still have P.O.T.S. or are my symptoms caused by the cardiac issues?
- Is there any way to know the cause of the pericardial effusion?
- Was there a blockage in the arteries?
- What is the treatment?
- Why did I only show an abnormal heart rhythm after exercise?
- Should I continue to salt-load and water-load, even though that is against cardiac treatment but good for P.O.T.S.?
- Should I still wear the compression socks?
- Why did these abnormalities not show on any EKG?
- Do I have sustained or nonstained ventricular tachycardia?
- Is the tachycardia polymorphic or monomorphic?
- Is there any evidence that I’ve had a heart attack?
- Could the ventricular tachycardia be causing the low ejection fraction?
- Do I have diastolic or systolic heart failure?
- Could the cardiac issues be causing the gastrointestinal symptoms?
- Other questions:
- Will I still go to the Dysautonomia Clinic at University Hospital?
- Should I get a second opinion from vascular surgery?
- Could any of this be related to neurotransmitters or hormones?
- particularly, catecholamine and cortisol levels?
- What s the likelihood I have an infiltrative disease or autoimmune disease?
- Most important question:
I had visions of the doctor literally picking me up and throwing me out of the office, shortly followed my “scroll” of questions. I highly doubted that it would actually happen, but you never know these days. It’s was a lot to ask. I typically try to keep both my medical concerns and my list of questions to five or less each, respectively. However, I felt this was super important and I needed to know. I opted to take my chances.
The night before my follow-up appointment with the cardiologist I could barely sleep.
There were too many things running through my mind. Do I have everything I need? What am I forgetting? What do I do if he says [this]? What if they tell me [that]? I literally drove myself crazy just over thinking everything. I knew I needed sleep more than anything. It was an hours drive again and I was scheduled first thing at 7:30 a.m. I think I finally fell into sleep somewhere around 3:00 a.m. before my alarms went off at 5:00 a.m. I was too anxious to need much sleep anyway, the adrenaline kept me awake that morning on the drive anyway.
We arrived at the clinic that morning, early as usual.
It wasn’t long after we checked in that we were escorted back to the exam room. From there, though, we had a wait, which is unusual for this clinic. We wait in silence as 5 minutes go by, then 10, and 20. You could feel the anxiety and tension build up in the tiny exam room as we waited on the cardiologist. I could see my husband getting impatient, it’s all over his face. I, myself, feel like I’m going to explode inside. I don’t dare to breathe. Just when I can’t take it anymore, the doctor walks in.
I take a deep breath. My palms are sweaty. My heart is beating.
I just want to get this over with.
Red = Abnormal results
The Echocardiogram With Agitated Saline:
Left Ventricle: No regional wall motion abnormalities noted. The left ventricle
cavity size is normal. Left ventricular systolic function is mildly reduced. Normal left ventricular diastolic function with normal LA pressure. Left ventricular wall thickness is normal. There are false chords noted in the left ventricle
[Had to look this up, as I had no idea what it meant: “Left ventricular (LV) false chordae tendinae (false chords) have been implicated as a source of idiopathic left (IL) ventricular tachycardia (VT). However, it is unknown whether pretest bias contributes to an apparent association with disease. The purpose of this study was to determine the prevalence of false chords on direct inspection of the LV endocardium”.]
Right Ventricle: Global RV systolic function is normal with a tricuspid annular
plane excursion of 1.76 cm. Right ventricular size is normal.
Left Atrium: The left atrium is normal in size with a left atrial volume index of
Right Atrium: The right atrium is normal in size. Eustachian valve seen in the
right atrium (normal finding).
[Of personal note here, I looked up to see why this would be noted like this and I found this:
“Eustachian Valve: It is a remnant of a fetal structure that directed incoming oxygenated blood to the foramen ovale and away from the right atrium.
Incomplete regression of this structure results in a thickened ridge at the IVC/RA junction, which can occasionally be thick enough to mimic thrombus or a right atrial mass on echocardiography, cardiac CT, or cardiac MRI.
A thickened Eustachian valve may also interfere with placement of an atrial septal defect or patent foramen ovale closure device.
The Eustachian valve can be seen in the 4-chamber view or the bi cavil view of the right atrium; it is seen in approximately 25% individuals, at the junction of the IVC and right atrium. It appears as an elongated, membranous, possibly undulating structure. Usually it is of no physiological consequence, but can be confused with an intracardiac thrombus, cause turbulent atrial blood flow, complicate IVC cannulation or serve as a site for endocarditis formation”.]
Aortic Valve: The aortic valve was not well visualized. No evidence of aortic
regurgitation is seen. No evidence of aortic valve stenosis.
Mitral Valve: Trace mitral valve regurgitation. No mitral valve prolapse is noted.
Tricuspid Valve: Grossly normal. Unable to estimate Right Ventricular systolic
pressure due to inadequate or absent TR Doppler signal. There is trace tricuspid
Pulmonic Valve: The pulmonic valve was not well visualized. No pulmonic valve
stenosis. Trace pulmonic valve regurgitation.
Vessels: IVC is normal in size with normal inspiratory collapse suggesting a normal
right atrial pressure (3) rnrnHg.
Aorta: The aortic arch was not well visualized. Aortic root is normal in size. No
obvious coarctation of the aorta noted by 20, Doppler.
Pericardium: No definite echocardiographic evidence of hemodynamic compromise. There is a moderate pericardial effusion localized near the right ventricle.
Shunts: There is no obvious right to left shunt at rest, with cough, or Valsalva on
agitated saline contrast examination.
The Holter Monitor:
1. Sinus rhythm, predominantly sinus tachycardia, with rates between 61-190
bpm and average rate 101 bpm .
2. Supraventricular ectopy: One isolated PAC in 24 hrs.
3. Ventricular ectopy: One, isolate 7 beat run ~f monomorphic ventricular
tachycardia with irregular rate 169 pm at 11:59 AM; otherwise, no other
4. Longest R-R was 1.2 seconds during sinus arrhythmia.
5. Symptoms of “fatigue, faint, abdominal pain, dizzy, chest pressure, chest
pain, flutter, chest tightness, pre– syncope,” and patient events all correlated
with sinus tachycardia, and in particular, the symptom of “pre-syncope” correlated with sinus tachycardia 185 bpm; with the 7 beat run of monomorphic ventricular tachycardia was asymptomatic.
The Exercise Stress Test:
1. Fair age- and gender-adjusted exercise capacity.
2. No evidence for exercise-induced ischemic ECG changes at the level of
3. Normal HR response (patient held Metoprolol for 48+ hours prior to exercise,
normal BP response. Target heart rate was achieved.
4. Pulse oximetry readings were greater than or equal to 95% on room air
throughout -the study.
Note: The baseline ECG reveals sinus tachycardia, rate of 107 bpm. ST-T shifts of ischemia or ectopy noted.
The Cardiac MRI w/ and w/o Contrast:
RESULT: Cardiac MRI
Clinical History: Pericardial effusion, cardiomyopathy. Evaluate LV function
delayed enhancement pattern
Technique: Following initial axial haste images, cine and dark blood images were
obtained in short axis, and vertical and horizontal long axis. 20 ml of ProHance
were administered intravenously, without adverse event. Immediate images were
obtained for perfusion. Delayed images were obtained in all 3 planes to evaluate
for delayed hyperenhancement. VIBE sequence was additionally acquired through the
The National Kidney Foundation (NKF) suggests only reporting actual results once values are < 60 mL/min (they state normal values as 90-120 mL/min). An eGFR below 60 mL/min suggests that some kidney damage has occurred.
|KIDNEY DAMAGE STAGE
||Normal or minimal kidney damage with normal GFR
||Protein or albumin in urine are high, cells or casts seen in urine
||Mild decrease in GFR
||Protein or albumin in urine are high, cells or casts seen in urine
||Moderate decrease in GFR
||Severe decrease in GFR
Survey images of the mediastinum show normal heart size. There is no pathologic mediastinal adenopathy or pleural effusion.
Atria: Right and left atria are normal in size and contract normally.
Right Ventricle: Right ventricle is normal in size. Globally preserved systolic function is preserved. No wall motion abnormality.
Left Ventricle: Normal size and wall thickness. Globally preserved systolic
function without wall motion abnormality.
Pericardium: Small pericardial effusion without evidence of constrictive physiology.
Perfusion images show: Homogenous perfusion without focal abnormality.
Delayed hyperenhancement images show: No delayed myocardial enhancement. Apparent focus of increased signal intensity seen at the lateral aspect of the base appears most consistent with a focus of epicardial fat when comparing to SSFP images and four-chamber and short axis sequences ( four-chamber series 3 image 59, short axis series 57 images 1 through 3) .
Left ventricular ejection fraction: 59%
End diastolic volume: 84 ml
End systolic volume: 34 ml
Stroke-volume: 50 ml
Cardiac output: 4.2 liters per minute
Left ventricular myocardial mass (at ED): 59 g
Right ventricular ejection fraction: 51%
No delayed myocardial enhancement to suggest infiltrative cardiomyopathy.
Preserved LV systolic function without wall motion abnormality.
Small pericardial effusion without evidence for constrictive physiology.
Nichole returns following her initial visit with me on 07/08/2015. At that time, we had performed an echocardiogram to assess for LV size, systolic function and possible pericardial effusion. This revealed the presence of a moderate size effusion without clear evidence of hemodynamic compromise. Also surprising was the presence of borderline reduced LV systolic function.. Based upon these findings, a cardiac MRI was run and revealed preserved LV systolic function, EF 59%, with normal left ventricular end diastolic and systolic volumes. RV ejection fraction was also normal at 51%. There was a small pericardial effusion which was circumferential and without clear evidence of septal shift or other stigmata of constrictive physiology. Also surprising was the presence of what was identified to be a 4-beat run of wide complex tachycardia which occurred at a rate of 169 beats per minute at 12:00 a.m. There were no associated symptoms. There were multiple entries recording complaints of fatigue, faint abdominal pain, dizzy, chest pressure, chest pain, flutter, chest tightness and presyncope, all of which were correlated with sinus tachycardia. Based upon these findings, we start Nichole on metoprolol XL 25 mg daily, which she initially felt somewhat more fatigued and dizzy on, but since that time has adjusted to. She has also made a more concerted effort to use volume and sodium loading, for which she feels better overall from a POTS standpoint. She continues to report left-sided chest pain, which is not necessarily positional in nature.
REVIEW OF SYSTEMS:
Positive for weight gain, fatigue, loss of appetite, chills, dizziness, nosebleed, shortness of breath, chest pain, palpitations, near fainting/fainting, leg cramps, abdominal pain, diarrhea, constipation, nausea, vomiting, blood in stool, rash, itching, nighttime urination, snoring, back pain, muscle aches and joint aches. Comprehensive review of
other 12-organ review of systems is otherwise negative.
Epinephrine caused adverse reaction.
1. Pericardial effusion in the context of presumed autoimmune disorder not otherwise specified, possibly lupus with negative antinuclear antibody (ANA), undergoing further evaluation with [Immunology]. Pericardial effusion does not appear to be associated with constrictive physiology by echocardiographic criteria. This is likely chronic in
nature. I cannot exclude the possibility of chronic pericarditis as a contributing cause to her chest discomfort.
2. Probable postural orthostatic tachycardia syndrome (POTS), complicating #1.
3. New onset wide complex tachycardia, possibly ventricular tachycardia. I cannot exclude atrial dysrhythmia with aberrancy tolerating beta blocker therapy, with associated preserved left ventricular (LV) systolic function by magnetic resonance imaging (MRI), which is gold standard data for ventricular volumes and function.
4. Prior history of superior mesenteric artery (SMA) syndrome and May-Thurner syndrome.
1. Referral to Dr. [Vascular Surgery] at the University cardiovascular center for a second opinion.
2. Consider initiation of low-dose ibuprofen. I will discuss this plan of care with Drs. [gastroenterology] and [immunology] to ensure that this is appropriate from their perspectives.
3. Continue beta blocker therapy for ventricular tachycardia versus supraventricular tachycardia (SVT) with aberrancy with monitoring symptoms.
4. Return to clinic in three months’ time for clinical reassessment.
5. Repeat echocardiogram in three months’ time for reassessment of pericardial effusion, particularly should we initiate nonsteroidal anti-inflammatory drug (NSAID) therapy.
6. Avoid prednisone therapy due to potential provocation of a relapsed pericarditis.
7. Collaborative care with Drs. [gastroenterology] and [immunology].
The good news: My heart is not failing like they originally thought on the left side. In fact, my ejection fractions are higher on the left than the right.
The bad news: Looks like there are some valvular problems with blood flow, but only mildly. Also, there are a few structural and/or congenital abnormalities which have led me to some further research that is quite interesting, but I won’t post until I’ve got a few more pieces together and have talked to the doctor about it.
Finally, there’s no significant answers or treatment plan at this time. At this point we are continuing medications as previously prescribed. Both the GI and the Immunology doctors gave the go ahead to start 200mg Ibuprofen twice a day (although right before this test I was on 800mg ibuprofen one time a day for bleeding following my endometrial ablation – which means it probably won’t reduce the pericardial effusion, but we’ll see).
The cardiologist does not want to start me at the dysautonomia clinic until he is sure that the effusion is not contributing to my POTS symptoms, although he doubts that it is. He still firmly believes I have P.O.T.S. or some form of dysautonomia, but he doesn’t want to send the referral just to get sent right back over something he should be handling on his own anyway. Still no idea what could be causing the pericardial effusion, but the cardiologist continues to believe it is something autoimmune related (due to its chronic nature), despite what the immunologist now says about having zero indications for autoimmune disease (even though that wasn’t what she told me) but not sure if we’ll ever find it if it is. Did a random skin biopsy on my arm last week when I had a “vasculitis-type rash”, but it came back inconclusive as well. I should know more when I get the report when I get the sutures out of Tuesday.
The cardiologists did, however, give me a referral for a second opinion from vascular surgery at University. I think he has some ideas on some of the research I am contemplating as well, but he won’t say at this time. He put my order in as “Urgent”. The new hospital called a couple of days later to schedule, but I couldn’t get the other hospitals to send records and scans over it time for the appointment. We rescheduled with them for this upcoming Tuesday. I’m hoping they can shed more light on the impact of the compression disorders or, at the very least, believe they exist (which they do).
It’s been a whirlwind couple of weeks as far as medical stuff goes. While I’m tired and ready for a break, at least we’re getting somewhere and I’m not going to die like I thought after the first few phone calls from the cardiologist’s office. My heart is not “normal”, so it’s not good news but it’s not bad either. So far, the Metoprolol is not helping the tachycardia, but I am still on a low dose and I really need to call the doctor and see if we can do an increase. So while this is the end of the chaos with cardiology, at least for now, it’s only the beginning for so many other new doctors and appointments.