Amlodipine-Induced Schamberg DiseaseKey Clinical MessageAmlodipine, a commonly prescribed antihypertensive agent, can rarely cause Schamberg disease. Recognition of this drug-induced etiology is essential, as discontinuation of the offending medication alone may result in complete resolution and prevent unnecessary investigations or prolonged treatment.IntroductionSchamberg disease, also known as progressive pigmented purpuric dermatosis, is the most common subtype of pigmented purpuric dermatoses. It is characterized by non-blanching petechiae and brownish macules resulting from capillaritis with erythrocyte extravasation and hemosiderin deposition. Although most cases are idiopathic, associations with systemic conditions and medications have been reported. Calcium channel blockers, particularly amlodipine, are widely used antihypertensive agents but are rare triggers of Schamberg disease.Case History and ExaminationA woman in her 30s with newly diagnosed essential hypertension was started on amlodipine 5 mg once daily. Approximately 3 to 6 weeks after initiation, she developed multiple pinpoint red macules over both feet and ankles, progressing into non-blanching petechial and brownish macules with a characteristic cayenne-pepper appearance as shown inFigure 1 and Figure 2 . She denied pruritus, pain, systemic symptoms, bleeding manifestations, recent infections or trauma. Physical examination revealed symmetrical non-blanching petechiae and hyperpigmented macules over the dorsum of both feet. No edema, ulceration or signs of venous insufficiency were noted.Differential Diagnosis, Investigations, and TreatmentThe differential diagnosis included leukocytoclastic vasculitis, thrombocytopenic purpura, stasis dermatitis and other variants of pigmented purpuric dermatoses. Laboratory investigations including complete blood count, platelet count and coagulation profile were within normal limits. Based on the characteristic clinical appearance, temporal relationship with amlodipine initiation and exclusion of alternative diagnoses, a diagnosis of amlodipine-induced Schamberg disease was made. Amlodipine was discontinued and replaced with an alternative antihypertensive agent. No topical or systemic therapies were initiated.Conclusion and Results (Outcome and Follow-Up)Following discontinuation of amlodipine, the lesions gradually faded over 4 to 8 weeks, with near-complete resolution by three months. No recurrence was observed on follow-up and blood pressure remained well controlled on alternative therapy.DiscussionDrug-induced Schamberg disease is uncommon but has been described in association with several medications, including calcium-channel blockers. Proposed mechanisms include immune-mediated capillaritis, endothelial dysfunction and increased capillary fragility. A representative histopathology image demonstrating the characteristic capillaritis pattern of Schamberg disease is shown in Figure 3 (6). The strong temporal association between amlodipine exposure and symptom onset, coupled with resolution after drug withdrawal, supports a causal relationship in this case. Recognition of medication-induced Schamberg disease is clinically important, as withdrawal of the offending agent alone may lead to resolution, avoiding unnecessary diagnostic procedures and prolonged treatment. Given the widespread use of amlodipine, clinicians should maintain awareness of this rare but reversible adverse cutaneous reaction.Patient ConsentWritten informed consent was obtained from the patient for publication of this case report and accompanying clinical images.References1. Zhang L, et al. Pigmented purpuric dermatoses: a review. Clin Dermatol. 2019. 2. Cox NH. Purpura and bleeding due to calcium-channel blockers. Clin Exp Dermatol. 2002. 3. Schetz D, Kocić I. Schamberg’s disease caused by amlodipine administration: a case report. Br J Clin Pharmacol. 2015. 4. Singh G, et al. Amlodipine-associated Schamberg disease. Am J Ther. 2022. 5. Ranugha PSS, et al. Cutaneous adverse reactions to antihypertensive drugs. Indian J Dermatol Venereol Leprol. 2014. 6. Al Kiyumi MH, et al. Rutoside and ascorbic acid in the treatment of Schamberg pigmented purpuric dermatosis. Cureus. 2021;13(6):e15833.

When Trabeculations Disrupt Conduction: Left Ventricular Noncompaction Presenting with High-Grade Atrioventricular BlockKey Clinical MessageLeft ventricular noncompaction cardiomyopathy (LVNC) should be considered in young patients presenting with unexplained arrhythmias. Cardiac MRI is critical for definitive diagnosis when echocardiographic findings are equivocal. Management focuses on clinical manifestations rather than myocardial morphology. Rhythm surveillance and risk stratification for sudden cardiac death are essential for follow-up.AbstractLeft ventricular noncompaction cardiomyopathy (LVNC) is an uncommon and heterogeneous myocardial disorder characterized by excessive trabeculation and deep intertrabecular recesses, believed to arise from abnormal myocardial compaction during embryogenesis. Clinical presentation ranges from asymptomatic disease to heart failure, malignant arrhythmias, thromboembolism and sudden cardiac death. Advanced atrioventricular (AV) conduction disease is an infrequent but clinically important manifestation. We report the case of a young woman presenting with dizziness and symptomatic bradycardia who was found to have high grade AV block with left bundle branch block morphology. Transthoracic echocardiography suggested apical trabeculation with preserved systolic function, while cardiac magnetic resonance imaging (CMR) established the diagnosis by demonstrating a markedly elevated noncompacted-to-compacted myocardial ratio and mildly reduced left ventricular ejection fraction. This case underscores the importance of multimodality imaging, heightened clinical suspicion in young patients with unexplained conduction disease and contemporary management aligned with guideline-directed therapy.IntroductionLeft ventricular noncompaction cardiomyopathy (LVNC) is classified as a distinct cardiomyopathy by the European Society of Cardiology and is characterized by prominent myocardial trabeculations and deep intertrabecular recesses that communicate with the ventricular cavity. The prevailing hypothesis attributes LVNC to arrest of normal myocardial compaction during early embryogenesis, although adaptive and acquired mechanisms have also been proposed. Genetically, LVNC is highly heterogeneous, with pathogenic variants most frequently involving sarcomeric and cytoskeletal genes such as MYH7, TTN, MIB1 and TAZ[1,2].The reported prevalence of LVNC varies widely, from <0.1% in population-based echocardiographic studies to over 10% in selected cohorts, reflecting differences in diagnostic criteria, imaging modalities and referral bias [3]. Clinically, LVNC demonstrates marked phenotypic variability. Patients may remain asymptomatic or present with heart failure, ventricular and supraventricular arrhythmias, thromboembolic events, or sudden cardiac death [4]. Although arrhythmias are common, advanced AV conduction disease remains a relatively rare and incompletely characterized presentation [5].We present a case of LVNC in a young adult with high-grade AV block, highlighting diagnostic challenges, the central role of CMR, and management considerations relevant to contemporary clinical practice.Case PresentationPresenting Complaints and Disease HistoryA young woman in her 30s presented to the emergency department with acute onset dizziness, lightheadedness, and nausea. Her medical history was notable for post traumatic stress disorder. She denied prior cardiovascular disease, chest pain, dyspnea or palpitations, although she recalled remote syncopal episodes during adolescence. There was no known family history of cardiomyopathy or sudden cardiac death.On presentation vital signs demonstrated sinus bradycardia. A 12-lead EKG revealed sinus rhythm with high grade AV block (Figure 1), with left bundle branch block accelerated ventricular escape rhythm. Heart rate declined progressively from approximately 63 beats per minute on arrival to the low 40s during inpatient monitoring.