Coronary Artery Stenosis and Its Psychological Impact - Cardiology

Coronary artery stenosis / psychoneurosis / trapezius muscle syndrome?

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Hello Dr.
Wu, I apologize for the complexity and length of my questions and symptoms; it requires some time to digest.
About three years ago, after a car accident, I began experiencing symptoms such as panic-like episodes, palpitations, and brief chest pain (sharp pain in specific muscle locations) about a month later, prompting me to consult a cardiologist.
At the time of the accident, I had no injuries, only vehicle damage.
A 24-hour Holter monitor, exercise stress test, and echocardiogram showed no abnormalities.
I was prescribed Alprazolam 0.25 mg, Tensocaine, and Inderal 10 mg to take as needed.
For muscle pain, I underwent traction and electrical therapy at a rehabilitation clinic, which provided effective relief.
Within a month, the symptoms disappeared, only to be replaced by gastrointestinal issues.
Later, a health check and endoscopy revealed the presence of a gastric ulcer (in the healing phase with intestinal metaplasia), while the colon showed no abnormalities.
After four months of treatment with pantoprazole, follow-up endoscopy confirmed healing.
Subsequently, I experienced intermittent pain in the right upper abdomen.
At 36, I had my gallbladder removed due to bile duct obstruction, but an ultrasound showed no abnormalities, leading to the belief that my symptoms were stress-induced irritable bowel syndrome.
For several months, I managed symptoms with loperamide and fludiazepam.
This cycle tends to recur approximately once a year.
Each time I experienced palpitations, I visited the cardiology clinic, where the 24-hour Holter monitor again showed no abnormalities.
For extended periods, I primarily dealt with gastrointestinal symptoms, with occasional gastric symptom recurrences.
Follow-up endoscopies revealed mild gastric lesions, which improved with PPI treatment.
I also controlled intestinal spasms with medication when symptoms arose.
During episodes of panic and palpitations, I experienced more severe neurological symptoms, such as unilateral limb numbness, difficulty speaking and breathing, and unilateral facial weakness or involuntary twitching.
Brain CT and MRI revealed a small pituitary tumor and an intramedullary vascular malformation, which were deemed non-symptomatic and did not require treatment.
Endocrinology and neurology consultations also indicated normal findings, with rehabilitation noting common cervical spine alignment issues, suggesting possible autonomic dysfunction.
Panic and palpitations typically last less than a month, while gastrointestinal symptoms can persist for several months, managed through dietary control and regular exercise.
I have long believed this to be a case of somatoform disorder or autonomic dysfunction and have tried traditional Chinese medicine, maintaining a normal diet and exercise routine.
I even experienced facial herpes zoster, but prompt treatment alleviated most symptoms within one to two months.
However, after being diagnosed with COVID-19 at the end of last year and the beginning of this year (twice, with less than three months apart), I noticed different developments.
The first time, I only had noticeable palpitations and almost no upper respiratory symptoms.
The second time was more typical and lasted longer, but the symptoms were generally not severe; I only consulted a cardiologist via video during the first diagnosis and took Inderal.
In early this year’s cardiology check-up (annual follow-up), the 24-hour Holter monitor was normal, but the exercise stress test revealed slight abnormalities: abnormal ST junction and segment shift (three consecutive beats), with a junction depression of 1 mm and downsloping ST segment from the J point for at least 0.08 seconds, observed in leads III and aVF.
The comment noted that myocardial ischemia could not be completely ruled out.
A Tl-201 myocardial perfusion scan was subsequently performed, which also showed some abnormalities.
The attending physician suggested mild hypoxia.
Other areas were thought to be close to the stomach/diaphragm, showing significant color differences.
The findings included: 1.
Mild severity, reversible perfusion defects in the basal anterolateral wall, mid posterior wall, and apex of the left ventricle, suggesting stress-induced myocardial ischemia.
2.
Moderate severity, reversible perfusion defects in the basal inferoseptal wall of the left ventricle, suggesting stress-induced myocardial ischemia.
3.
Fixed perfusion defects in the basal anterior wall, basal anteroseptal wall, basal inferolateral wall, mid inferoseptal wall, mid inferior wall, and mid inferolateral wall of the left ventricle, suggesting myocardial ischemia.
4.
Reverse redistribution of thallium activity in the basal inferior wall and apical inferior wall of the left ventricle, possibly due to damaged myocardium.
The summed stress score was 12, and the summed rest score was 10.
A coronary CT angiogram was performed next: RCA showed evidence of mixed plaques with 25-29% (mild) lumen stenosis in segment 1, mixed and calcified plaques with 0-24% (minimal) lumen stenosis in segments 1 and 2, mixed and calcified plaques with 25-49% (mild) lumen stenosis in segments 2 and 3, and mixed plaques with 50-70% (moderate) lumen stenosis in segment 2.
The PDA showed no evidence of atherosclerotic plaque or stenosis.
The left main artery showed no abnormalities, while the left anterior descending artery had mixed plaques with 50-70% (moderate) lumen stenosis in segment 6, calcified plaques with 0-24% (minimal) lumen stenosis in segment 8, and mixed plaques with 25-49% (mild) lumen stenosis in D1.
The left circumflex artery had calcified plaques with 25-49% (mild) lumen stenosis in segment 11 and 0-24% (minimal) lumen stenosis in segment 12.
The PDA originates from the RCA.
The coronary artery calcium score was: LM: 0, LAD: 82, LCX: 10, RCA: 286, PDA: 2, Total: 380.
Other areas, including the aorta and pericardium, showed no abnormalities.
Wow, there are multiple lesions in all three arteries.
The results heightened my anxiety.
I have a long history of elevated low-density lipoprotein cholesterol (>100), which was >120 six years ago.
My high-density lipoprotein cholesterol is around 50, and my total cholesterol has been approximately 180 for the past two to three years due to dietary and exercise control, with low-density lipoprotein around just over 100.
However, annual health checks show a cardiovascular risk of less than 1%.
Last year, I even had a carotid ultrasound, and the slight narrowing of the left carotid artery found five years ago has returned to normal, which I attributed to exercise and weight control.
There is no significant family history of cardiovascular disease.
Therefore, the results surprised the physicians (not just one).
They could only attribute it to stress and chance.
My attending physician has currently started medication treatment and observation: Beraprost 100 mg, Kanekon 1.25 mg twice daily, and Lipitor 20 mg.
Further treatment will depend on observation and my subjective symptom assessment.
However, I have a tendency toward somatoform disorder, making me easily tense (previously managed with Inderal and Alprazolam).
Various neuropathic and tendon pains caused by the left trapezius are alleviated with Tensocaine.
The combination of somatoform disorder and left shoulder issues has created a feedback loop that causes discomfort, especially after confirming cardiovascular lesions (which were not as pronounced before confirmation).
I even went to the emergency room due to this.
Therefore, my subjective awareness seems unreliable.
After several weeks/months of observation and reflection, I noticed that my pain and tension occur in atypical angina areas, and nitroglycerin is ineffective, but the aforementioned medications (Tensocaine and Alprazolam) provide effective relief.
For palpitations, I take Kanekon long-term.
However, when faced with significant stress or fatigue, tension or muscle/fascial pain arises, and the current dosage seems insufficient, but I am hesitant to increase it.
At rest, such as during the night, I do not experience symptoms.
Symptoms most commonly occur after a full day of work (mostly in the afternoon).
Continuing activities like walking and climbing stairs do not exacerbate the symptoms, but resting does not easily alleviate them, requiring a longer recovery time or direct medication (Alprazolam/Tensocaine) for relief.
During my last follow-up, my attending physician noted that based on the exercise stress test and myocardial perfusion scan, the degree of coronary artery stenosis should not correlate with such significant pain or tension symptoms, so I remain under observation.
My observation is that palpitations from higher intensity exercise (maintaining a heart rate above 100 at rest for up to half an hour without pain or shortness of breath) seem more indicative of true myocardial hypoxia.
However, even the physician cannot guarantee this.
I am now hesitant to jog and only walk for over 30 minutes daily.
Due to the prolonged process of confirming the lesions, I have developed a dependency on Alprazolam after taking it continuously for three months.
Attempts to taper the medication have resulted in noticeable withdrawal symptoms, and I currently cannot stop, trying to take it only when symptoms arise, totaling 0.5 mg per day.
I take Tensocaine almost daily for tendon pain caused by tension.
Rehabilitation has been temporarily halted due to the importance of addressing the heart lesions.
I feel that continuing Alprazolam is not a solution, as it was initially intended for short-term anxiety relief.
When larger stressors or burdens arise, increasing the dosage does not seem to be a good approach.
The symptoms of stenosis appear to be in a gray area where treatment is difficult to define.
I would like to ask Dr.
Wu: 1) Even if my tension and pain symptoms are not caused by cardiovascular lesions, would you recommend preventive coronary artery stenting to alleviate psychological burdens in my case? 2) If stenting is performed, drug-eluting stents require prolonged anticoagulation therapy; is this appropriate? (I have already started taking aspirin regularly, and I am currently on a PPI or H2 blocker to prevent gastric issues, planning to taper off if I experience no discomfort for a period.) 3) If stenting leads to restenosis, is it possible to discern this in my situation? For a man in his early 40s, completely eliminating external stress is unlikely.
I have already begun adjusting my routine as much as possible.
However, I find myself in a dilemma between passively taking medication and seeking more aggressive treatment for frequently occurring symptoms.
Thank you very much, Dr.
Wu, for reading through this lengthy account, and I would appreciate any suggestions you may have.

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Niming, 40~49 year old female. Ask Date: 2023/05/25