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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

ParameterValue
PatientP. Thakur, Age ~41, Female
BMI26
HbA1c5.4
eGFR1.95
Trop I~0.05
LDL82
TG159
T.Chol129
Duke Score(documented)
AccessRadial (RA) @HP (200)
Opening BP120/66 mmHg, HR 86/min
Closing BP110/70 mmHg
SpO299%

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

SegmentFindings
LM (Left Main)Normal
LAD - ProximalNormal
LAD - MidNormal, slow flow noted
LAD - DistalNormal
LAD - DiagonalNormal
LAD - SeptalNormal
LCx - OstiumNormal
LCx - ProximalNormal
LCx - OM (Obtuse Marginal)Normal
LCx - DistalNormal
LCx - PDNormal
LCx - PLVNormal

Right Coronary System

SegmentFindings
RCA - ProximalNormal, "dyskinesia/thrombus?" noted
RCA - MidSlow flow, noted
RCA - DistalNormal
RCA - PDNormal
RCA - PLVNormal
RV BranchNormal

Dominance

  • Left dominant circulation (circled on report)

TIMI Frame Count (TFC) - Key Finding

VesselTFC
c-LAD32
LCx21
RCA26
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:
  1. Epicardial coronary spasm (noted in report as "Epicardial coronary spasm")
  2. Normal coronaries (no obstructive CAD)
  3. Slow flow in LAD and RCA
  4. 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)

ParameterFinding
ProjectionLAO 30° / Cranial 4°
Contrast@5cc/ml, 25 flow, 500 PSI
LV SizeNormal
LV Opens intoAorta (normal)
LV ContractionNormal (grade 4+)
WallPosteriorly placed ventricular chamber, smooth walled
Aortic Annulus30 mm
Ascending Aorta26 mm (mildly dilated/normal upper limit)
MRTrace/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:
  1. No obstructive coronary artery disease - all vessels angiographically smooth
  2. Coronary Slow Flow Phenomenon - confirmed by elevated TFC (LAD = 32, borderline RCA = 26)
  3. Epicardial coronary spasm - documented explicitly
  4. Endothelial dysfunction - underlying mechanism
  5. Mild Mitral Regurgitation with MVP - pre-existing valve lesion
  6. Mildly elevated LVEDP (16 mmHg) - consistent with diastolic dysfunction
  7. 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

ItemValue
SmokerNo (circled)
DMNo (circled)
HTN~41 years (age confirmed)
CADYes (noted)
CKDNo
CKDP?
CVAPositive, eye (likely prior CVA or eye symptom noted)
NeuroparesisPositive (circled - likely peripheral neuropathy or paresis noted)

Presenting Complaint

c/o Chest pain at ~3 AM, 19/6/26

Local Examination of Chest Pain

FeatureDescription
OnsetSudden onset
LocationBilateral / central (circled "both sides")
RadiationNon-radiating
IntensityMild
DurationLasting 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:
DomainFinding
Chief complaintSudden onset bilateral non-radiating mild chest pain at 3 AM
Syncope1 episode - brief LOC, no premonitory symptoms, self-fall, no post-ictal features
Old CVA2020 - documented prior stroke history
Cath findingsNormal coronaries, coronary slow flow (TFC: LAD 32), epicardial spasm, endothelial dysfunction
ValveMild MR with MVP
LVNormal systolic function, LVEDP mildly elevated (16 mmHg)
Risk factorsNon-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:
  1. Vasovagal syncope (most common in young women) - but nocturnal onset at 3 AM is atypical
  2. Arrhythmic syncope - needs Holter/ECG monitoring; vasospasm can trigger arrhythmia
  3. Vertebrobasilar insufficiency - given old CVA history
  4. 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

FieldDetails
NameSanjay 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:
  1. Worsening SOB (Shortness of Breath) - NYHA Class I/m (possibly progressing from Class I to moderate - likely NYHA II)
  2. Effort intolerance - worsening
  3. 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

FeatureDetail
SOBNYHA Class II, worsening over 1 month
Effort intoleranceProgressive - uphill walking → 3-4 flight of stairs
Pre-syncopeNew - 2 days, concerning symptom
No orthopnea/PNDSuggests not yet decompensated into NYHA III-IV
No RHF signsNo 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:
  1. Low fixed cardiac output - severe MR/MS reducing forward flow
  2. Arrhythmia - AF is extremely common in RHD/mitral disease; can cause pre-syncopal episodes
  3. 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:
  1. Urgent echocardiography (or review of 2023 CORT study) to assess current valve gradient, MR severity, LV dimensions and EF
  2. Holter monitoring - to evaluate for AF or other arrhythmias causing pre-syncope
  3. Cardiology review for mitral valve intervention (repair or replacement) given severe MVD + severe LVSD - surgical threshold consideration
  4. 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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