47 F recurrent ADHF with inflammatory myocarditis
Age / Sex: 47-year-old female
Comorbidities: Type 2 Diabetes Mellitus
Late July / August 2025 (Initial Presentation)
Chief Complaints: Giddiness, a single episode of transient loss of consciousness (LOC) lasting approximately 2 minutes, and one episode of vomiting.
Pre-Hospital Course: Evaluated at an outside facility where she received an acute coronary syndrome (ACS) loading dose consisting of Acetylsalicylic Acid (Ecosprin) 325 mg, Clopidogrel (Clopitab), and Atorvastatin (Atorva) 80 mg prior to transfer.
Emergency Department Presentation: The patient demonstrated profound bradycardia with a pulse rate of 40 bpm and initial hypotension measuring 100/60 mmHg, necessitating immediate inotropic and supplemental oxygen support. Following initial stabilization, vitals normalized to a blood pressure of 130/70 mmHg, respiratory rate of 20/min, and an $SpO_2$ of 98% on room air.
Physical Examination: Systemic evaluation revealed adequate bilateral air entry, normal S1/S2 heart sounds without murmurs, a soft abdomen with intact bowel sounds, and no gross focal neurological deficits.
Laboratory and Diagnostics:
Hematology: Hemoglobin 11.50 g/dL, Total Leukocyte Count (TLC) elevated at 11,110 /µL, Platelet count 3.15L.
Cardiac Biomarkers: Significantly elevated extra-sensitive Troponin-I at 1.20 ng/mL (Reference cut-off: 0.12 ng/mL) and highly elevated NT-proBNP.
Etiological Screening: Serum Angiotensin-Converting Enzyme (ACE) was normal at 54 U/L; Anti-Nuclear Antibody (ANA) profile and Anti-Mitochondrial Antibody (AMA-M2) were both negative; Liver and Renal Function Tests were within normal limits.
Echocardiography Screening: Demonstrated regional wall motion abnormalities (RWMA) of the left ventricle (LV) and mild LV systolic dysfunction.
Interventional Procedures:
Temporary Pacemaker Implantation (TPI) & Coronary Angiogram (CAG): Emergent TPI was secured via the right femoral vein with the lead positioned at the right ventricular (RV) apex, programmed to a backup rate of 80 bpm. A concurrent diagnostic CAG via the right radial artery revealed completely normal epicardial coronary arteries within a left-dominant coronary system (LMCA normal, LAD Type 3 normal, LCX dominant/normal, RCA non-dominant/normal).
Permanent Pacemaker Implantation (PPI): Given a definitive diagnosis of Complete Heart Block (CHB), the patient underwent an uneventful dual-chamber PPI (Boston Scientific Accolade MRI EL DR) via the left subclavian route. The device was programmed to DDD mode (Lower rate 60 bpm, Max tracking rate 130 bpm). Intracardiac parameters were excellent (Right Atrium: threshold 0.8V, P/R wave 4.1mV, impedance 567 $\Omega$; Right Ventricle: threshold 0.6V, P/R wave 11.4mV, impedance 784 $\Omega$).
Formal Post-Procedure Echocardiogram: Confirmed status post-dual chamber PPI, concentric LV hypertrophy (LVH), persistent regional wall motion abnormalities, mild LV systolic dysfunction, and mild tricuspid regurgitation (TR) with mild pulmonary artery hypertension (PAH).
Hospital Course & Disposition: Stabilized in the Intensive Coronary Care Unit (ICCU) with supportive care including a course of antibiotics, NSAIDs, and successful weaning of inotropes. Discharged in a hemodynamically stable condition.
Resident Clinical Insight:
The initial presentation strongly mimicked an obstructive acute myocardial infarction due to the combination of high-grade conduction failure, elevated Troponin-I (1.20 ng/mL), and distinct regional wall motion abnormalities on echocardiography. However, the angiographically pristine epicardial coronaries coupled with normal serum ACE and negative initial autoimmune markers pointed toward a non-atherosclerotic process—initially interpreted as demand-driven ischemia (Type 2 Myocardial Infarction) due to profound bradycardic shock.
ADMISSION 2: August 31, 2025 – Early September 2025 (Acute Decompensation)
Chief Complaints: Progressive shortness of breath (SOB) Grade-II starting on August 30, 2025, which acutely aggravated on the morning of August 31, 2025.
Clinical Presentation: The patient was tachycardic at 124 bpm, hypotensive with a systolic blood pressure of 90 mmHg, and hypoxic with an SpO_2 of 94% on room air.
Working Diagnosis: Lower Respiratory Tract Infection (LRTI), Cardiogenic Shock, Status Post PPI (completed August 11, 2025), Severe LV Dysfunction, and Acute Inflammatory Myocarditis.
Diagnostic Workup:
Bedside Abdominal Ultrasound (01/09/2025): Noted significant congestive hepatomegaly measuring 17.9 cm, a partially distended gallbladder with a 3.4 mm mobile echogenic focus (? calculus) and wall thickening of 4.8 mm, and very minimal free fluid in the pelvis.
Cardiac FDG PET-CT Scan (05/09/2025): The perfusion scan confirmed a dilated LV cavity with global hypokinesia and moderate-to-severe perfusion deficits involving 32% to 34% of the LV myocardium (specifically the anteroseptal, mid-anterior, basal anterior, mid-anterolateral, apical septal, and part of the apical lateral segments). The metabolic PET findings demonstrated a profound perfusion-metabolic mismatch, showing mild, homogeneous increased tracer uptake across the entire right ventricle and left ventricle, with intense focal uptake in the inferior wall ($SUV_{max}$ 3.0) and the basal anterior segment ($SUV_{max}$ 2.8). Calcified or metabolically active mediastinal lymphadenopathy was absent.
Metagenomic Analysis (Virfast): A specialized blood metagenomic screen identified the molecular presence of Simbu orthobunyavirus (Score: 41).
Resident Clinical Insight:
The discovery of Simbu orthobunyavirus via metagenomic sequencing completely recontextualized the case. This confirmed that the complete heart block requiring a permanent pacemaker weeks prior was not degenerative, but rather the initial clinical manifestation of a rare, viral-induced inflammatory cardiomyopathy that rapidly progressed from localized AV-nodal disease to diffuse biventricular fulminant myocarditis and secondary cardiogenic shock.
ADMISSION 3: Mid-to-Late September 2025 (Electrical Storm & Renal Strain)
Chief Complaints: Worsening SOB and persistent giddiness for 1 month, accompanied by a productive cough for 1 week.
Clinical Presentation: Blood pressure was stabilized at 120/70 mmHg, pulse rate was 90 bpm, and pulmonary auscultation revealed bilateral basal crepitations consistent with volume overload.
Electrocardiogram & Echocardiography: Telemetry caught frequent runs of Non-Sustained Ventricular Tachycardia (NSVT) interrupting an intermittent pacing rhythm. A repeat echocardiogram demonstrated worsening structural remodeling: persistent biventricular wall motion deficits, severe LV systolic dysfunction, and dramatic thinning of the anterior myocardium down to a thickness of 4 mm.
Hospital Course & Secondary Complications:
The patient presented in Acute Decompounded Heart Failure (ADHF) and was stabilized with aggressive intravenous diuresis and CPAP support.
Acute Kidney Injury (AKI): Developed secondary cardio-renal syndrome type 1 or acute tubular necrosis; serum creatinine was tracked sequentially, showing an acute rise from 1.45 mg/dL (16/09) to a peak of 2.44 mg/dL (19/09), which successfully resolved down to 1.26 mg/dL by discharge following targeted nephrology adjustments.
Metabolic/Infectious Status: Concurrently treated for a documented Urinary Tract Infection (UTI) amid poor baseline glycemic control (HbA1c: 8.9%).
Therapeutic Re-alignment & Discharge Advice: Following a multidisciplinary rheumatology and cardiology consensus tracking the persistent hypermetabolic focus on the prior PET scan, a provisional diagnosis of chronic inflammatory cardiomyopathy/suspected cardiac sarcoidosis was maintained, and the patient was initiated on oral corticosteroids (Tab. Wysolone 15 mg OD). To suppress the malignant ventricular arrhythmia burden, dual antiarrhythmic therapy was started with Metoprolol XL, Amiodarone, and Mexiletine. Plans were formally documented to upgrade the existing system to a Cardiac Resynchronization Therapy Defibrillator (CRT-D) at a later date.
ADMISSION 4: October 2025 (Neuromuscular & Glycemic Decompensation)
Chief Complaints: Bilateral lower limb swelling tracking upwards from the ankles for 15 days, coupled with progressive, severe weakness in both lower extremities.
Clinical Presentation: Soft blood pressure readings at 90/60 mmHg, heart rate of 76/min, dry exfoliating skin over the lower limbs, and pitting edema localized to the right forearm. Neurological exam confirmed isolated proximal muscle weakness (Neck flexor power 4/5, proximal lower limb flexors 4/5), while distal motor function remained intact at 5/5.
Advanced Investigations:
Cardiovascular Status:
The Holter monitor (14/10/25) verified stable baseline pacemaker tracking with a controlled average heart rate of 94 bpm and a minimal ventricular ectopic burden (49 isolated bimorphic VPCs, zero runs of NSVT/SVT), validating the efficacy of the antiarrhythmic regimen.
The baseline LVEF had dropped to 25% with global hypokinesia and persistent 4 mm anterior wall thinning.
Pulmonary Architecture: A High-Resolution CT (HRCT) of the chest demonstrated early interstitial pulmonary edema, peribronchovascular ground-glass opacities (GGOs), interlobular septal thickening, cardiomegaly, a mild pericardial effusion, and early calcifications within the mediastinal lymph nodes.
Autoimmune / Serological Profiling: A new comprehensive serology panel revealed a highly significant positive ANA Immunofluorescence Assay (Intensity 2+, Homogeneous pattern) with clear specificity for anti-dsDNA and anti-histone antibodies. Crucially, a full Myositis Immunoblot Profile (Mi-2, Jo-1, SRP, MDA5, PL-7/12) returned entirely negative, and serum Creatine Phosphokinase (CPK) was normal at 96 U/L.
Neuromuscular Imaging & Electrophysiology: An Electroneuromyography (ENMG) study demonstrated an isolated sensory neuropathy (absent left sural SNAP, reduced right sural SNAP amplitude).
An MRI of Bilateral Thighs demonstrated prominent muscle bulk reduction and extensive fatty infiltration across the gluteal and vastus muscle groups, combined with extensive, asymmetric intrasubstance STIR hyperintensity (edema) matching a radiologic pattern of active myositis.
Metabolic Status: Glycemic control completely collapsed, with the patient's HbA1c skyrocketing to 16.4%.
Hospital Course & Management Taper: The patient's presentation represented a complex diagnostic overlap of active systemic autoimmune disease (SLE/Lupus-Myositis vs. Drug-Induced Lupus from antiarrhythmics) vs. steroid-induced proximal myopathy and steroid-unmasked severe diabetes mellitus. The treating team optimized her heart failure therapy by initiating Sacubitril/Valsartan (Tab. Arney 50 mg BD) and an SGLT2 inhibitor (Tab. Oxra 10 mg OD). Given the severe proximal weakness and an HbA1c of 16.4%, the systemic corticosteroid dose was carefully tapered down to Tab. Wysolone 10 mg OD, and urgent endocrine titration was mandated.
ADMISSION 5: January 2026 (Thrombotic and Arrhythmic Relapse)
Chief Complaints: Recurrent, severe acute shortness of breath secondary to volume overload.
Clinical Presentation: Tachycardic at 112 bpm, blood pressure 110/60 mmHg, and an $SpO_2$ of 94% on room air. The patient did not exhibit gross peripheral edema or icterus at this presentation.
Cardiovascular and Lab Evaluation:
Electrolyte Crisis: Chemistry panels on admission (25-01-2026) revealed an acute hypokalemia of 3.0 mmol/L and hypocalcemia at 1.08 mmol/L.
Arrhythmia Recurrence: This low potassium threshold broke electrical stability, provoking an acute recurrence of an NSVT run captured via telemetry. Intravenous electrolyte replacement ($KCl$ and $MgSO_4$) successfully restored her serum potassium to 4.1 mmol/L, terminating the ventricular runs. Renal parameters remained stable with a serum creatinine of 1.0 mg/dL.
Vascular Complication: Due to asymmetric upper limb signs and a history of indwelling hardware, a venous Doppler was performed, revealing a new partial chronic thrombus involving the right Internal Jugular Vein (IJV) extending into the right axillary vein. The patient was immediately started on therapeutic anticoagulation.
Neuromuscular Progression: Following up on upper extremity symptoms, a High-Resolution Ultrasound (HRUS) of the left ulnar nerve was ordered. It demonstrated marked structural pathology, including focal thickening and hypo-echogenicity of the left ulnar nerve ($16\text{ mm}^2$ cross-sectional area at the cubital fossa, tapering to $4\text{ mm}^2$ at the wrist). The dorsal cutaneous branch at the wrist was also abnormally thickened ($6\text{ mm}^2$) and hyper-echogenic, which had already resulted in moderate fatty atrophy of the hypothenar muscles.
Disposition: The patient was successfully compensated from a heart failure perspective using intravenous diuresis and temporary inotropic support. Pacemaker interrogation confirmed appropriate device functionality. She was transitioned back to oral medical therapy and discharged in a stable condition with detailed counseling regarding her guarded long-term prognosis.
Resident Clinical Insight:
The fifth admission ties the vascular and neurological elements together. The right IJV/axillary vein thrombus represents a classic macrovascular hardware complication (lead-associated thrombosis) from the permanent pacemaker system placed in August 2025. However, given her previous serology (ANA positive, anti-dsDNA positive), this thrombotic event—alongside the sonographically confirmed left ulnar mononeuropathy with muscle atrophy—strongly underscores a systemic, active autoimmune vasculopathy or secondary antiphospholipid phenomenon that continues to drive multi-organ pathology alongside her end-stage 25% dilated cardiomyopathy.
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