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coronary slow flow TIMI frame count epicardial coronary spasm endothelial dysfunction management 2024
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I now have enough information to provide a thorough interpretation of this catheterization report. Here is the full analysis:
Cardiac Catheterization Report - Interpretation
Institution: Department of Cardiology, AIIMS Chamiana, Shimla, H.P.
Operators: Dr. Bikesh/Vinay (Fellow) / Dr. Pravin (Consultant)
Patient & Procedural Data
| Parameter | Value |
|---|---|
| Patient | P. Thakur, Age ~41, Female |
| BMI | 26 |
| HbA1c | 5.4 |
| eGFR | 1.95 |
| Trop I | ~0.05 |
| LDL | 82 |
| TG | 159 |
| T.Chol | 129 |
| Duke Score | (documented) |
| Access | Radial (RA) @HP (200) |
| Opening BP | 120/66 mmHg, HR 86/min |
| Closing BP | 110/70 mmHg |
| SpO2 | 99% |
Pre-procedure Diagnosis
- MR (Mitral Regurgitation) - mild (Grade I)
- MVP (Mitral Valve Prolapse) with AVL (likely aortic valve lesion or anterior leaflet involvement)
- Clockwise rotation MR
- Chief complaint: Chest pain
Coronary Angiography Findings
Vessels accessed: LMCA, LCA/RCA, FA (femoral/radial approach), AORTA views
Left Coronary System
| Segment | Findings |
|---|---|
| LM (Left Main) | Normal |
| LAD - Proximal | Normal |
| LAD - Mid | Normal, slow flow noted |
| LAD - Distal | Normal |
| LAD - Diagonal | Normal |
| LAD - Septal | Normal |
| LCx - Ostium | Normal |
| LCx - Proximal | Normal |
| LCx - OM (Obtuse Marginal) | Normal |
| LCx - Distal | Normal |
| LCx - PD | Normal |
| LCx - PLV | Normal |
Right Coronary System
| Segment | Findings |
|---|---|
| RCA - Proximal | Normal, "dyskinesia/thrombus?" noted |
| RCA - Mid | Slow flow, noted |
| RCA - Distal | Normal |
| RCA - PD | Normal |
| RCA - PLV | Normal |
| RV Branch | Normal |
Dominance
- Left dominant circulation (circled on report)
TIMI Frame Count (TFC) - Key Finding
| Vessel | TFC |
|---|---|
| c-LAD | 32 |
| LCx | 21 |
| RCA | 26 |
Interpretation: Normal TFC cutoff is LAD ≤21, LCx/RCA ≤14-27 (depending on reference). A cTFC >27 is diagnostic of Coronary Slow Flow Phenomenon (CSFP). The LAD TFC of 32 is elevated, confirming slow flow in the LAD. RCA of 26 is borderline. LCx of 21 is within normal limits.
Summary of Angiographic Impression
The report explicitly states:
- Epicardial coronary spasm (noted in report as "Epicardial coronary spasm")
- Normal coronaries (no obstructive CAD)
- Slow flow in LAD and RCA
- Endothelial dysfunction
This constellation is consistent with Coronary Vasospastic Angina / Microvascular Angina - the patient has chest pain with angiographically normal coronaries but demonstrable slow flow (elevated TFC) and spasm, pointing to vasomotor dysfunction rather than obstructive CAD.
Left Ventriculography (LV Angio)
| Parameter | Finding |
|---|---|
| Projection | LAO 30° / Cranial 4° |
| Contrast | @5cc/ml, 25 flow, 500 PSI |
| LV Size | Normal |
| LV Opens into | Aorta (normal) |
| LV Contraction | Normal (grade 4+) |
| Wall | Posteriorly placed ventricular chamber, smooth walled |
| Aortic Annulus | 30 mm |
| Ascending Aorta | 26 mm (mildly dilated/normal upper limit) |
| MR | Trace/mild |
LV Pressures:
- LVP 120/16 mmHg (normal LVEDP 16 mmHg is slightly elevated, suggests mild diastolic dysfunction or volume overload consistent with mild MR)
RWMA (Regional Wall Motion Abnormality) Assessment
- RVMA/LAD/LCx/RCA territories: Noted as with EF in RVLR/SF CivcLV region - likely documenting 2 apical/anterior wall motion segments assessed
- No significant RWMA documented
Overall Clinical Interpretation
This is a middle-aged woman (~41 years) presenting with chest pain, found to have:
- No obstructive coronary artery disease - all vessels angiographically smooth
- Coronary Slow Flow Phenomenon - confirmed by elevated TFC (LAD = 32, borderline RCA = 26)
- Epicardial coronary spasm - documented explicitly
- Endothelial dysfunction - underlying mechanism
- Mild Mitral Regurgitation with MVP - pre-existing valve lesion
- Mildly elevated LVEDP (16 mmHg) - consistent with diastolic dysfunction
- Normal LV systolic function with smooth-walled ventricle
Diagnosis: Coronary Vasospastic Angina / Coronary Microvascular Disease (CMD) with Coronary Slow Flow Phenomenon
Clinical Significance & Management Considerations
- CSFP with TFC >27 in LAD is an independent predictor of adverse cardiac events despite "normal" angiography
- Treatment typically includes: calcium channel blockers (first line for vasospasm), nitrates, possibly statins (even with low LDL, for pleiotropic effects on endothelial function), and nicorandil
- The troponin of ~0.05 (borderline/mildly elevated) and HbA1c 5.4 (prediabetes range) are contributory risk factors for endothelial dysfunction
- The MVP with mild MR warrants periodic echocardiographic surveillance but no intervention at this stage
*This interpretation is based on careful reading of the handwritten cath report from AIIMS Chamiana. Some values may require confirmation directly from the original document.*This appears to be a clinical history and physical examination sheet for the same patient. Let me read it carefully and provide a full interpretation.
Clinical History & Physical Examination - Page 2
Document type: Inpatient case sheet (handwritten), page 2
Date of complaint: 19/6/26 at ~3 AM
Top Right Corner - Quick Summary Box
| Item | Value |
|---|---|
| Smoker | No (circled) |
| DM | No (circled) |
| HTN | ~41 years (age confirmed) |
| CAD | Yes (noted) |
| CKD | No |
| CKDP | ? |
| CVA | Positive, eye (likely prior CVA or eye symptom noted) |
| Neuroparesis | Positive (circled - likely peripheral neuropathy or paresis noted) |
Presenting Complaint
c/o Chest pain at ~3 AM, 19/6/26
Local Examination of Chest Pain
| Feature | Description |
|---|---|
| Onset | Sudden onset |
| Location | Bilateral / central (circled "both sides") |
| Radiation | Non-radiating |
| Intensity | Mild |
| Duration | Lasting few minutes |
Per Abdominal & Per Rectal Examination
- c/o: Old CVA (possibly old cerebrovascular accident history noted - dated 2020)
- Abdominal and rectal examination otherwise unremarkable (NAD / OHP documented)
Cardiovascular System Examination
- No chest pain (at time of examination - ruling out active ischemia)
- No palpitations
- Had 1 episode of syncope - significant finding
Respiratory System Examination
- Brief episode of LOC (loss of consciousness) for few seconds
- She self-fell with no regard of fall concern
- No palpitations / exertion / positional change (ruling out orthostatic, exertional, or positional triggers)
Nervous System Examination
- No premonitory symptoms (no aura, no warning before syncope)
- Not after:
- Seizure
- Weakness (limb)
- Incontinence
- Blurring of vision (These features effectively rule out an epileptic seizure or TIA as cause of the LOC)
Musculo-skeletal System
- No h/o:
- Paralysis
- Active bleeding
- Insulin use (confirms no diabetes requiring insulin)
Endocrinal System
- P/H (Past History): NAP (Not a problem / no relevant history)
- F/H (Family History): Negative
Synthesis with Previous Cath Report
Combining both documents, the full clinical picture is:
| Domain | Finding |
|---|---|
| Chief complaint | Sudden onset bilateral non-radiating mild chest pain at 3 AM |
| Syncope | 1 episode - brief LOC, no premonitory symptoms, self-fall, no post-ictal features |
| Old CVA | 2020 - documented prior stroke history |
| Cath findings | Normal coronaries, coronary slow flow (TFC: LAD 32), epicardial spasm, endothelial dysfunction |
| Valve | Mild MR with MVP |
| LV | Normal systolic function, LVEDP mildly elevated (16 mmHg) |
| Risk factors | Non-smoker, non-diabetic, non-hypertensive (paradoxically low-risk profile) |
Key Clinical Concern
The syncope episode with no premonitory symptoms, brief LOC, self-fall, combined with a history of old CVA (2020) and now coronary vasospastic angina / CSFP raises important differentials:
- Vasovagal syncope (most common in young women) - but nocturnal onset at 3 AM is atypical
- Arrhythmic syncope - needs Holter/ECG monitoring; vasospasm can trigger arrhythmia
- Vertebrobasilar insufficiency - given old CVA history
- Neurocardiogenic syncope in the setting of autonomic dysfunction (which is also linked to endothelial dysfunction and CSFP)
The nocturnal chest pain at 3 AM is a classic time for coronary vasospasm (vagal tone peaks at night), strongly supporting Prinzmetal/variant angina as the unifying diagnosis.
*Interpretation based on handwritten clinical notes. Some words may require verification against the original document.*This is a different patient - a General Case Sheet from Atal Institute of Medical Super Specialities (AIMOS), Shimla. Let me read it carefully.
General Case Sheet - AIMOS Shimla (Page 3)
Institution: Atal Institute of Medical Super Specialities, Shimla - 171 012 (H.P.)
Patient Demographics
| Field | Details |
|---|---|
| Name | Sanjay Kumar, 44y / M (Male) |
| CR No. | 9.21.5126.00.28.1409 |
Chief Complaints with Duration
c/o:
- RHD (Rheumatic Heart Disease) with mild MR (Mitral Regurgitation) + Severe MVD (Mitral Valve Disease) / Severe LVSD (Left Ventricular Systolic Dysfunction)
- Duration: Stagnant ~3 years (noted as "3 yrs" with "blue" - possibly bluish discoloration/cyanosis)
- CORT (2023) - likely a previous cardiac study/report from 2023
- (7) Study - possibly a 7th follow-up study
Right-side box:
- Smoker: Positive (circled)
- HTN: Present
- CAD: Positive (circled)
- CVA: Noted
- CKD: Noted
History of Present Illness
c/o:
- Worsening SOB (Shortness of Breath) - NYHA Class I/m (possibly progressing from Class I to moderate - likely NYHA II)
- Effort intolerance - worsening
- Pre-syncope - x 2 days (new symptom, 2 days duration)
Note: Patient presently had SOB NYHA II
Past History of Illness / Surgical Operation / Interventions
- Had worsening SOB for last 1 month
- Gradually progressive - initially on walking uphill
- Now occurs on climbing 3-4 flights of stairs
- NYHA II - No orthopnea / PND (Paroxysmal Nocturnal Dyspnea) / No RHF (Right Heart Failure) symptoms
History of Drug or Other Allergies
- c/o effort intolerance - worsening (reiterated)
Family History
- Dyspnea on walking uphill / climbing stairs
- No h/o chest pain / palpitations
- No h/o cold intolerance / constipation (ruling out hypothyroidism)
- No h/o active bleeding
Clinical Interpretation
This is a 44-year-old male smoker with known Rheumatic Heart Disease (RHD) presenting with:
Primary Diagnosis
RHD with Severe Mitral Valve Disease (MVD) + Severe LV Systolic Dysfunction (LVSD)
Presenting Syndrome
| Feature | Detail |
|---|---|
| SOB | NYHA Class II, worsening over 1 month |
| Effort intolerance | Progressive - uphill walking → 3-4 flight of stairs |
| Pre-syncope | New - 2 days, concerning symptom |
| No orthopnea/PND | Suggests not yet decompensated into NYHA III-IV |
| No RHF signs | No peripheral edema, no JVD documented here |
Why Pre-syncope is Concerning Here
In a patient with severe mitral valve disease + severe LVSD, pre-syncope can indicate:
- Low fixed cardiac output - severe MR/MS reducing forward flow
- Arrhythmia - AF is extremely common in RHD/mitral disease; can cause pre-syncopal episodes
- Progression to hemodynamic compromise - a red flag for urgent intervention consideration
Risk Factor Profile
- Smoker - accelerates cardiac remodeling
- HTN - adds pressure load on already dysfunctional LV
- CAD mentioned - coexisting ischemic component possible
- No diabetes, no hypothyroidism (ruled out by history)
- No active bleeding - relevant for anticoagulation planning (RHD patients in AF need warfarin)
Clinical Priority
This patient likely needs:
- Urgent echocardiography (or review of 2023 CORT study) to assess current valve gradient, MR severity, LV dimensions and EF
- Holter monitoring - to evaluate for AF or other arrhythmias causing pre-syncope
- Cardiology review for mitral valve intervention (repair or replacement) given severe MVD + severe LVSD - surgical threshold consideration
- Anticoagulation if AF confirmed
This is a separate patient from the previous cath report. Two different cases from the same institution.
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Usage of this drug and side effects
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Tendocare Forte L-Arginine collagen peptides sodium hyaluronate chondroitin sulfate uses side effects
Reading Web Page
https://www.practo.com/medicine-info/tendocare-tablet-58542
Here is a complete breakdown of Tendocare Forte:
Tendocare Forte - Complete Drug Profile
Manufacturer: Pharmed Ltd.
Category: Nutraceutical / Nutritional Supplement (not a steroid, not a scheduled drug)
Pack: 15 tablets
Composition (per tablet)
| Ingredient | Role |
|---|---|
| L-Arginine | Amino acid; precursor to nitric oxide; promotes blood flow and tissue healing |
| Collagen Peptides Type I | Structural protein for tendons, ligaments, cartilage, bone, and skin |
| Sodium Hyaluronate | Lubricates and cushions joints; retains water in connective tissue |
| Chondroitin Sulfate | Proteoglycan component of cartilage; reduces cartilage breakdown |
| Vitamin C (Ascorbic Acid) | Essential co-factor for collagen synthesis; antioxidant |
Uses / Indications
- Tendon & ligament injuries - the primary indication (the name "Tendo-care" reflects this); supports repair of tendons after sprains, tears, or overuse injuries
- Osteoarthritis - reduces pain and swelling from joint cartilage wear; improves flexibility
- Post-surgical joint recovery - aids soft tissue healing after orthopedic procedures
- Sports injuries - used by athletes for connective tissue repair and prevention of re-injury
- Joint pain & stiffness - reduces friction in joints through hyaluronate lubrication
- Cartilage degeneration - slows breakdown of joint cartilage
- Skin, hair, and nail health - collagen peptides support dermal structure
How It Works (Mechanism)
- L-Arginine → converts to nitric oxide (NO) → vasodilation → improved blood supply to tendons and healing tissue (tendons are naturally avascular, making this especially useful)
- Collagen Peptides Type I → provides amino acid building blocks (glycine, proline, hydroxyproline) for tendon/cartilage matrix synthesis
- Sodium Hyaluronate → binds water molecules in synovial fluid → acts as a shock absorber and lubricant within joints
- Chondroitin Sulfate → inhibits enzymes that break down cartilage; stimulates proteoglycan synthesis by chondrocytes
- Vitamin C → essential for hydroxylation of proline and lysine in collagen cross-linking; without it, collagen synthesis is incomplete
Dosage
- Typical dose: 1 tablet once or twice daily, with food
- Duration: Usually 3-6 months for joint/tendon conditions (nutraceuticals need time to show effect)
- As directed by physician
Side Effects
Common (Mild)
| Side Effect | Notes |
|---|---|
| Nausea / Vomiting | Take with food to minimize |
| Diarrhoea | Usually self-limiting |
| Bloating / gas | From chondroitin sulfate |
| Headache | Mild, infrequent |
| Flushing / skin redness | Due to L-Arginine (vasodilatory effect) |
| Increased urination | From Vitamin C (diuretic effect at high doses) |
Serious (Rare)
| Side Effect | Notes |
|---|---|
| Kidney stones | Vitamin C at high doses can increase oxalate excretion - use with caution in those with kidney stone history |
| Haemolytic anaemia | Risk in G6PD deficiency patients - Vitamin C can precipitate red cell breakdown |
| Bleeding risk | Chondroitin sulfate can potentiate the effect of Warfarin/anticoagulants - monitor INR closely |
| Allergic reaction | Rare; if rash, urticaria, or breathing difficulty - stop immediately |
Contraindications & Cautions
| Condition | Advice |
|---|---|
| Warfarin / anticoagulant use | Avoid or use with close monitoring - chondroitin increases bleeding risk |
| History of kidney stones | Use with caution; ensure adequate hydration |
| G6PD deficiency | Caution - risk of haemolytic anaemia from Vitamin C |
| Pregnancy | Safety not established - consult doctor |
| Breastfeeding | Safety not established - consult doctor |
| Hypotension | L-Arginine lowers blood pressure via NO - caution with antihypertensives |
| Recent MI (heart attack) | L-Arginine supplementation should be avoided post-MI (some evidence of harm) |
| Shellfish allergy | Chondroitin is often derived from shellfish - check source |
Drug Interactions
| Drug | Interaction |
|---|---|
| Warfarin (Anisindione) | Chondroitin significantly potentiates anticoagulant effect - risk of serious bleeding |
| Antihypertensives / nitrates | L-Arginine may cause additive blood pressure lowering |
| Antidiabetics | L-Arginine can affect insulin secretion - monitor blood sugar |
Key Points to Remember
- It is not a painkiller - it does not provide immediate pain relief like NSAIDs; it works over weeks to months by rebuilding tissue
- It is not a steroid - no hormonal or immunosuppressive effects
- Best taken with food to reduce GI side effects
- Staying well hydrated is recommended to reduce kidney stone risk
- Most side effects are mild and resolve on stopping the medication
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