60M Acute Left Femoral Artery Embolism Secondary to Large Left Ventricular Outflow Tract and Mitral Valve Vegetations in a Patient with Hypertrophic Cardiomyopathy

 

60M with Acute Left Femoral Artery Embolism Secondary to Large Left Ventricular Outflow Tract and Mitral Valve Vegetations in a Patient with Hypertrophic Cardiomyopathy: A Case Report

Case Presentation

A 60-year-old male resident of Hyderabad and retired employee presented with severe pain in the left lower limb. According to the available records, the pain had an insidious onset and progressively worsened over approximately three days. An outside Doppler examination reportedly demonstrated left femoral artery thrombosis, and the patient was referred for further management.  

His past medical history was significant for:

• Hypertrophic cardiomyopathy (diagnosed in 2010)
• Left ventricular outflow tract obstruction with mitral valve involvement
• Previous infective endocarditis (as documented in the presentation material)
• Type 2 diabetes mellitus
• Hypertension
• Hypothyroidism
• Obesity with obstructive sleep apnea
• Chronic smoking history
• Prior history of left femoral artery thrombus/embolus documented in the medical records  

Physical Examination

On admission, the patient was conscious and coherent.

Recorded vital signs included:

• Pulse rate: 102 beats/min
• Blood pressure: 130/90 mmHg
• Respiratory rate: 20/min
• Temperature: 98.4°F
• Oxygen saturation: 93% on room air

The absent palpable pulses in the left anterior tibial and dorsalis pedis arteries with preserved limb warmth and no evidence of compartment syndrome or gangrene.  

Investigations

Transthoracic echocardiography demonstrated:

• Large vegetation within the left ventricular outflow tract
• Smaller vegetation on the left atrial aspect of the anterior mitral leaflet

https://youtu.be/fPauy0VKJjM ( TEE ) 

 

Laboratory data 

• Hemoglobin: 10.2 g/dL
• Serum creatinine: 1.12 mg/dL

Microbiological evaluation showed:

• Blood cultures: No bacterial growth
• Culture of embolic tissue obtained during embolectomy: No bacterial growth
• urine cultures were also negative.
• a septic panel identified Klebsiella species despite negative conventional cultures.
• 
  

PET CT ( whole body ) 

Management

The patient received treatment with:

• Intravenous antibiotics
• Heparin
• Diuretics
• Statin therapy
• Supportive medical management

Because of acute limb ischemia secondary to left femoral artery occlusion, he underwent emergency left femoral embolectomy under general anesthesia on 18 May 2026. Embolic material was submitted for histopathological examination and microbiological culture.  

https://youtube.com/shorts/4fAsxP8F3Dg?si=yEiDmhp09L-x6uNO

( femoral embolectomy )

The postoperative course was uneventful. The patient was extubated on the following day and remained hemodynamically stable.

Cardiothoracic surgery consultation recommended stabilization followed by definitive surgical management. Presentation records indicated a planned reassessment with transesophageal echocardiography and consideration of septal myectomy with mitral valve replacement or double-valve surgery depending on subsequent evaluation. 

coronary angiogram was done prior to surgery 

https://youtu.be/5JLTZzQv6vM?si=_HSPBwNYIC8Zg5FJ

patient underwent septal myomectomy with MVR. post MVR gradients

Gross Tissue sample of Mitral Valve and vegetation with septal tissue

 

patient extubated succesfully.  post extubation cardio respiratory physiotherapy and rehabilitation was done. 

tissue cultures are negative

on 26/7/2026, patient brought to ER with a/h/o sudden onset giddines, right upper and lowerlimb weakness and drowsiness,. 

A 60-year-old male with a history of hypertrophic obstructive cardiomyopathy (HOCM), status post mitral valve replacement (MVR) and septal myectomy, presented with acute neurological symptoms and was admitted for further evaluation and management.

Chief Complaints

• Giddiness
• Swaying to one side while walking
• Difficulty with gait/imbalance

Examination on Admission

The patient was drowsy but arousable to verbal commands.

• Pulse rate: 117/min
• Blood pressure: 90/60 mmHg
• Respiratory rate: 20/min
• Temperature: 98.4°F
• SpO₂: 98% on room air
• GCS: 15/15
• No pallor, icterus, clubbing, edema or cyanosis
• Cardiovascular examination: S1 and S2 present
• Respiratory examination: bilateral air entry present
• Abdomen: soft, bowel sounds present
• Neurological examination: no gross focal deficit documented initially; subsequent neuroimaging demonstrated cerebellar infarction.

Relevant Cardiac History

The patient had previously undergone mitral valve replacement and septal myectomy for HOCM. During the present admission, echocardiographic evaluation demonstrated a normally functioning prosthetic mitral valve with preserved ventricular systolic function.

Transthoracic Echocardiography

• HOCM, status post MVR and septal myectomy
• Echogenic specks on the mitral valve
• No significant valvular or paravalvular leak
• No obvious LV regional wall-motion abnormality
• Good LV systolic function
• Trivial TR
• No obvious LV clot
• IVC approximately 2.4 cm with >50% respiratory collapse

Transesophageal Echocardiography

TEE demonstrated:

• Status post MVR and septal myectomy
• Normally functioning prosthetic mitral valve
• Vegetation noted on the prosthetic mitral valve
• Additional vegetation involving the right coronary cusp (RCC) of the aortic valve
• Good biventricular systolic function
• Findings suggestive of early prosthetic valve infective endocarditis

Neurological Evaluation

CT brain showed no intracranial hemorrhage.

MRI brain subsequently demonstrated:

• Bilateral cerebellar infarcts
• Left middle cerebellar peduncle infarct
• Left superior cerebellar peduncle infarct

The clinical presentation of giddiness and gait imbalance was therefore consistent with acute cerebellar ischemic stroke. In the setting of prosthetic valve vegetation, the infarcts were considered likely embolic in nature.

Neurology consultation was obtained, and anticoagulation was advised after exclusion of intracranial hemorrhage.

Infective Work-up

A septic work-up was performed.

• Blood cultures: no growth
• Urine cultures: no growth
• Sepsis panel: no growth reported

Despite negative microbiological cultures, the echocardiographic demonstration of vegetation involving the prosthetic mitral valve, together with the clinical setting and embolic cerebral infarctions, raised strong suspicion for culture-negative / partially treated early prosthetic valve infective endocarditis.

Laboratory Investigations

Hematological Profile

There was persistent anemia with a microcytic/hypochromic pattern:

Parameter	31/07/2026	02/08/2026	04/08/2026
Hemoglobin	9.0 g/dL	8.4 g/dL	8.7 g/dL
RBC count	3.7 ×10⁶/µL	3.4 ×10⁶/µL	3.5 ×10⁶/µL
PCV	28.8%	26.4%	27.3%
MCV	77 fL	77 fL	76 fL
MCH	24 pg	24 pg	27 pg
MCHC	31 g/dL	31 g/dL	24 g/dL
RDW	14.5%	17.2%	17.2%
WBC	12,900/µL	9,700/µL	10,100/µL
Platelets	2.10 lakh/µL	2.13 lakh/µL	1.96 lakh/µL

The leukocytosis present initially subsequently improved.

Renal and Electrolyte Profile

• Creatinine was approximately 0.9–1.1 mg/dL during the earlier period.
• Creatinine subsequently increased to 2.32 mg/dL on 06/08/2026, consistent with an acute kidney injury during the hospital course.
• Potassium was repeatedly low, with values of 2.9 mmol/L on 04/08 and 05/08.
• Sodium remained within normal limits at approximately 141–144 mmol/L.
• Calcium was approximately 1.15–1.22 mmol/L as reported.

Coagulation Profile

The patient demonstrated marked anticoagulation during the later course:

Date	PT	INR
08/08/2026	30.3 sec	2.8
09/08/2026	51.8 sec	4.7
10/08/2026	41.4 sec	3.7

Control PT was 12 seconds.

The patient was receiving Acitrom (acenocoumarol) for prosthetic valve anticoagulation. The markedly elevated INR required close monitoring, particularly in view of concomitant antimicrobial therapy and renal dysfunction.

Liver Function / Protein Profile

Liver enzymes remained within normal limits:

• Total bilirubin: 0.36 mg/dL
• AST: 12 U/L
• ALT: 18 U/L
• Alkaline phosphatase: 113 U/L

There was hypoalbuminemia:

• Albumin: 3.3 g/dL
• Previous albumin values: 2.8–3.3 g/dL

Hospital Course

The patient was admitted with dizziness, gait imbalance and swaying to one side. Initial cardiac evaluation demonstrated preserved LV systolic function and a functioning prosthetic mitral valve. Given the neurological presentation, CT brain was performed and did not demonstrate intracranial hemorrhage.

MRI brain subsequently demonstrated cerebellar infarctions involving the bilateral cerebellum, left middle cerebellar peduncle and left superior cerebellar peduncle. The distribution was concerning for embolic ischemic stroke.

TEE was performed because of the prosthetic valve and demonstrated vegetations involving the prosthetic mitral valve and the RCC of the aortic valve, raising suspicion for early prosthetic valve infective endocarditis.

Blood and urine cultures remained negative. In view of the prosthetic valve vegetation and embolic neurological complications, the patient was managed as suspected culture-negative prosthetic valve endocarditis.

During hospitalization he received broad-spectrum antimicrobial therapy, including:

• Meropenem
• Vancomycin
• Rifampicin

He also received supportive treatment including IV fluids as clinically indicated, diuretics, statin therapy, non-invasive ventilatory support when required, and other supportive medications.

Neurology consultation was obtained. Following exclusion of intracranial hemorrhage, anticoagulation was continued/advised because of the prosthetic mitral valve and embolic stroke risk.

The hospital course was complicated by:

1. Acute kidney injury, with creatinine rising to 2.32 mg/dL.
2. Hypokalemia, with potassium as low as 2.9 mmol/L.
3. Supratherapeutic anticoagulation, with INR reaching 4.7.
4. Persistent microcytic anemia with hemoglobin around 8.4–9.0 g/dL.

The patient subsequently showed clinical improvement and was considered stable for discharge with continuation of antimicrobial therapy, anticoagulation and cardiac medications.

Final Clinical Impression

Primary Diagnosis

Suspected early prosthetic mitral valve infective endocarditis with culture-negative status and embolic cerebellar ischemic infarctions.

Associated Diagnoses

• Prosthetic mitral valve status post MVR
• HOCM status post septal myectomy
• Vegetation on prosthetic mitral valve
• Vegetation involving RCC of aortic valve
• Bilateral cerebellar infarctions with left middle and superior cerebellar peduncle involvement
• Acute kidney injury
• Hypokalemia
• Microcytic anemia
• Supratherapeutic anticoagulation
• Hypoalbuminemia

Discharge Medications

The discharge regimen included:

• Inj. Meropenem 1 g IV BD – planned for 4 weeks
• Inj. Vancomycin 1 g IV OD – planned for 4 weeks
• Rifampicin 600 mg orally OD – planned for 4 weeks
• Brevipil 50 mg BD
• Pantoprazole 40 mg OD
• Thyronorm 50 µg OD
• Metoprolol XL 25 mg BD
• Dytor 5 mg OD
• Dytor 2.5 mg OD
• Modalert 200 mg OD
• Aldactone 50 mg OD
• Ivabradine 5 mg BD
• Orofer-XT once daily
• Acitrom 0.5 mg/1 mg on alternate days, with INR monitoring

Condition at Discharge

At discharge, the patient was:

• Conscious and coherent
• Pulse: 80/min
• BP: 120/80 mmHg
• Temperature: 98.4°F
• Respiratory rate: 20/min
• SpO₂: 98% on room air
• No pallor, icterus, clubbing, edema or cyanosis

The patient was considered clinically improved and was discharged with advice for continued antimicrobial therapy, anticoagulation with close INR surveillance, neurophysiotherapy and speech therapy.

septic panel was sent in view of high TLC ~ 23k 

present admission (august 2026)

The patient was re-admitted after developing drowsiness, with laboratory investigations demonstrating hyponatremia.

The clinical significance of the hyponatremia is particularly important because the patient has a recent history of structural cerebellar ischemic injury and is receiving multiple medications, including diuretics and prolonged antimicrobial therapy.

The differential diagnosis for the altered sensorium includes:

1. Symptomatic hyponatremia
2. Metabolic encephalopathy related to renal dysfunction/uremia
3. Medication-related encephalopathy
4. Sepsis/infection-related encephalopathy
5. Recurrent or evolving cerebrovascular event
6. Intracranial bleeding, particularly in view of anticoagulation
7. Combined metabolic and neurological causes

Laboratory Trend

Hematological Parameters

The investigation chart demonstrates persistent anemia.

• Hemoglobin approximately 7.6–8.1 g/dL
• PCV approximately 23–24%
• Total leukocyte count approximately 6,000–8,500/µL in the documented serial values
• Platelet count approximately 2.1–3.7 lakh/µL

There is therefore significant persistent anemia without evidence of major thrombocytopenia.

Renal Function

Renal dysfunction persisted during the current clinical course.

Serial values demonstrated:

• Blood urea rising from approximately 80–84 mg/dL to 97 mg/dL
• Serum creatinine approximately 2.6–2.8 mg/dL in the later measurements

This represents persistent renal impairment and raises the possibility of a component of uremic/metabolic encephalopathy contributing to the patient’s drowsiness.

Serum Sodium

The most important biochemical abnormality during this admission was hyponatremia.

The available trend demonstrates:

• Previous sodium: 143 mmol/L
• Subsequent fall to approximately 128 mmol/L
• Later values: approximately 131–133 mmol/L
• Subsequent improvement toward 136 mmol/L

Thus, the patient developed a clinically significant decline in serum sodium from a previously normal baseline.

In the context of drowsiness, the possibility of symptomatic hyponatremia should be considered, although the degree to which hyponatremia alone accounts for the altered sensorium requires correlation with the rate of sodium decline and other metabolic/neurological findings.

Potassium

Potassium, which had previously been significantly low during the earlier admission, subsequently improved.

• Earlier value: approximately 2.9 mmol/L
• Subsequent values: approximately 4.1–4.5 mmol/L

Calcium

Ionized/serum calcium values remained approximately 1.13–1.19 mmol/L in the documented measurements.

Coagulation Profile

The patient remained on oral vitamin-K antagonist anticoagulation because of his prosthetic mitral valve.

The serial investigation chart demonstrates markedly labile anticoagulation, with several substantially elevated PT/INR measurements during the recent course.

This is clinically important because the patient now presents with drowsiness.

In an anticoagulated patient with altered sensorium and a recent history of cerebral infarction, intracranial hemorrhage must be actively excluded, even in the absence of obvious focal neurological deficits.

The markedly elevated INR values also require consideration of:

• Acenocoumarol effect
• Antibiotic–anticoagulant interactions
• Reduced oral intake/nutritional vitamin-K deficiency
• Acute kidney dysfunction
• Possible hepatic dysfunction
• Intercurrent infection/inflammation

Relevant Medication Exposure

The patient had recently been receiving:

• Meropenem
• Vancomycin
• Rifampicin
• Acenocoumarol
• Torsemide
• Spironolactone
• Metoprolol
• Ivabradine
• Other supportive medications

The combination of diuretic therapy, poor oral intake, renal dysfunction and ongoing systemic illness is particularly relevant when evaluating the new hyponatremia.

Clinical Assessment

The current admission represents a complex interaction between neurological, renal, metabolic and anticoagulation-related factors.

The immediate clinical concern is drowsiness in the setting of new/worsening hyponatremia.

Overall Clinical Problem List

1. Drowsiness/altered sensorium
2. Hyponatremia – nadir approximately 128 mmol/L
3. Acute/subacute kidney dysfunction – creatinine approximately 2.6–2.8 mg/dL
4. Azotemia – urea approximately 97 mg/dL
5. Recent bilateral cerebellar embolic infarctions
6. Recent suspected culture-negative prosthetic valve infective endocarditis
7. Prosthetic mitral valve
8. Ongoing anticoagulation with highly labile PT/INR
9. Severe persistent anemia – Hb approximately 7.6–8.1 g/dL
10. Recent history of hypokalemia, currently corrected
11. Ongoing prolonged antimicrobial therapy

The most important interaction map for this patient

Drug in chart	Expected effect on acenocoumarol/INR	Importance
Amiodarone	↑ anticoagulant effect → ↑ INR	🔴 Major
Fluconazole 200 mg	↑ anticoagulant effect → ↑ INR	🔴

Why is INR still 6.7 after Acitrom was withheld?

This is the key clinical point.

Think of it as:

Acitrom stopped
↓
No further drug entering the system

BUT

Existing pharmacodynamic anticoagulation
+
AMIODARONE inhibition
+
FLUCONAZOLE inhibition
+
acute severe illness
+
possibly poor nutrition/low vitamin K intake
+
possible hepatic dysfunction

↓

continued deficiency of functional II, VII, IX, X

↓

INR remains markedly elevated

So a persistently elevated INR does not mean that acenocoumarol is still being absorbed.

One particularly important clue in your chart

The INR values appear to fluctuate:

6.1 → 5.6 → 4.3 → 3.8 → 4.8 → 4.9 → 6.7

That pattern is more suggestive of ongoing interference/unstable vitamin-K antagonist physiology than simply residual acenocoumarol.

And the presence of both amiodarone and fluconazole is highly significant.