Cardiovascular Diseases

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  • Mostafa Elbanna, Fahad Eid, Mostafa Zaalouk, Ahmad Nawid Latifi, Gaurav Sharma
    Views: 49 HTML: 6 PDF: 32

    This report presents a 57-year-old female with a history of dyslipidaemia, intolerant to statins and currently managed on evolocumab. Despite a healthy lifestyle, lipid panel abnormalities persisted, leading to an investigation that revealed heterozygous mutations in the ABCG8 gene, confirming a diagnosis of sitosterolaemia. The patient’s unique response to lipid-lowering medications typified this rare disorder, necessitating specialised genetic testing for diagnosis. Management involved dietary modifications and the introduction of ezetimibe, evolocumab and atorvastatin, demonstrating the personalised nature of treatment. The case underscores the importance of considering sitosterolaemia in unexplained lipid abnormalities and highlights the challenges in diagnosis and management. Ongoing research is crucial for refining diagnostic and therapeutic strategies for this clinically significant disorder, emphasising the need for a multidisciplinary approach to patient care.

  • Devi Parvathy Jyothi Ramachandran Nair, Shilla Zachariah, Anisha Abraham, David Sacks, Michael Koslow, Rittu Hingorani
    Views: 178 PDF: 92 HTML: 8

    Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, the identification of such an anomaly led to the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH).
    A 49-year-old male with a history of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE) on anticoagulation presented with chest pain and shortness of breath. Laboratory analysis was remarkable for a troponin peak of 14.74 ng/ml, a brain natriuretic peptide level of 602 pg/ml and a D-dimer level of 0.62 µg/ml. Electrocardiogram showed non-specific ST elevation in the anterolateral and inferior leads. Computed tomography angiography (CTA) of the chest was positive for PE involving the right lower lobe pulmonary arterial tree. Echocardiogram showed reduced left ventricular function (ejection fraction 38%) and akinesis of the antero-apical and infero-apical segments. Cardiac catheterization revealed non-obstructive coronary arteries, and an anomalous origin of a right bronchial artery from the right coronary artery. The right bronchial hypertrophied as it supplied collateral flow to the occluded right pulmonary artery. This anomaly and the patient’s history of multiple DVT/PEs while on therapeutic levels of warfarin with near normal D-dimer levels raised suspicion for a false positive PE. Pulmonary angiogram revealed chronic occlusion in branches of the right pulmonary artery, mean pulmonary artery pressure of 36 mmHg and no acute thrombus. Ventilation-perfusion scan confirmed the diagnosis of CTEPH. The patient underwent successful pulmonary thromboendarterectomy and subsequently had normalization of mean pulmonary artery pressure.
    This case underscores the importance of a comprehensive diagnostic approach, and consideration of alternative explanations for imaging findings, that unveiled the diagnosis of a complex and life-threatening condition such as CTEPH.

  • Geeta Bhagia, Nasir Hussain, Fnu Arty, Mithun Chakravarthy, Moneal Shah
    Views: 140 HTML: 13 PDF: 84

    Background: Atypical myxoma has been reported in various locations in the heart, however, myxoma involving the pulmonary valve is rare. Here we present a case of pulmonic valve myxoma which was resected via a percutaneous approach.
    Case Report: A 66-year-old female with known metastatic adenocarcinoma of the lung, and chronic obstructive pulmonary disease presented with acute onset shortness of breath for two days. The patient experienced respiratory arrest en-route to the hospital and required intubation. Computed tomography angiography (CTA) of the chest revealed a new 1.4 x 1.6 cm intracardiac mass along the pulmonary valve. Further evaluation with cardiac magnetic resonance imaging revealed it to be a large vascular tumor on the ventricular side of the pulmonary valve, attached with a narrow stalk. Due to high surgical risk, the patient underwent transesophageal echocardiographic guided percutaneous removal of the mass. Pathology confirmed the mass to be a myxoma.
    Conclusion: Atypical myxoma should be considered in the differential diagnosis of valvular masses. Percutaneous resection of valvular masses may be feasible in high-risk surgical patients.

  • Zhafran Veliawan, Ardian Rizal, Indra Prasetya, Adhika Prastya
    Views: 127 HTML: 6 PDF: 67

    Inappropriate therapy is a frequent adverse consequence of implantable cardioverter-defibrillator. Inappropriate therapy often occurs due to the misinterpretation of sinus tachycardia or atrial fibrillation/flutter with rapid atrioventricular conduction by the device. Current implantable cardioverter-defibrillator (ICD) mechanisms integrate various discriminators into algorithms to differentiate supraventricular tachycardia (SVT) from ventricular tachycardia (VT), to prevent such occurrences. A 40-year-old man suffered seizures and cardiac arrest abruptly, without prior complaints of chest pain. Without delay, he initiated cardiopulmonary resuscitation (CPR), resulting in the regaining of spontaneous circulation. The patient had previously received a single-chamber ICD due to recurring VT and a prior episode of cardiac arrest. The patient had a medical background of coronary artery disease with complete revascularisation and no previous occurrence of SVT. Interrogating the ICD revealed captured non-sustained ventricular tachycardia (NSVT) and SVT events but no VT episode or shock therapy. During the specified time period, the patient underwent an electrophysiological study, and no SVT was induced with the normal function of the atrioventricular and sinoatrial nodes. Various causes can lead to errors in morphology discrimination criteria in single-chamber ICDs. Extending the detection interval is highly recommended to avoid misclassification of ICDs.

  • Geeta Bhagia, Nasir Hussain, Fnu Arty, Puneet Bansal, Robert Biederman
    Views: 169 HTML: 6 PDF: 83

    Background: Alagille syndrome (ALGS) is a multisystem disorder involving at least three systems among the liver, heart, skeleton, face, and eyes. Common cardiac associations include pulmonary artery stenosis/atresia, atrial septal defect (ASD), ventricular septal defect (VSD) and tetralogy of fallot (ToF). Coarctation of aorta (CoA), renal and intracranial arteries are commonly involved vessels in Alagille syndrome. We present two cases with rare cardiovascular manifestations of Alagille syndrome.
    Case description: Case 1: A 25-year-old female with a history of Alagille syndrome presented to the cardiologist office for progressive exertional dyspnoea, orthopnoea, and palpitations. She was tachycardiac on examination and had an apical diastolic rumble. A transthoracic echocardiogram (TTE) showed a left ventricular ejection fraction (LVEF) of 60% and parachute mitral valve (PMV) with severe mitral stenosis. A transoesophageal echocardiogram (TOE) showed insertion of chordae into the anterolateral papillary muscle, severe mitral stenosis with a valve area of 0.7 cm. She was referred to a congenital heart disease specialist and underwent robotic mitral valve replacement with improvement in her symptoms.
    Case 2: A 27-year-old female with known Alagille syndrome and resistant hypertension presented to the cardiologist office due to progressive exertional dyspnoea for a year. She was hypertensive and had a new 2/6 systolic ejection murmur along the left upper sternal border. TTE revealed an LVEF of 60% and pulmonary artery pressure of 19 mmHg. A CoA was suspected distal to the left subclavian artery due to a peak gradient of 38 mmHg. Cardiac magnetic resonance (CMR) imaging ruled out CoA, and diffuse narrowing of the descending thoracic aorta measuring 13–14 mm in diameter was noted. The patient was referred to a congenital heart disease specialist for further management.
    Conclusion: PMV presenting as mitral stenosis and mid-aortic syndrome are not commonly described anomalies in association with Alagille syndrome. TTE, TOE and CMR played a key role in diagnosis and management of these patients.

  • Dawood Shehzad, Mustafa Shehzad, Muhammad Ahmad, Abdul Wassey, Noor Zara, Humna Younis, Haider Ali Babar Khan
    Views: 149 HTML: 14 PDF: 123

    Introduction: Ventricular septal defect (VSD) is a severe complication following acute myocardial infarction (MI) resulting from mechanical disruption of the interventricular septum due to extensive myocardial necrosis. Despite advances in management, the mortality rate approaches 50%. We report a case of a 58-year-old male with VSD following MI who was successfully treated with a delayed surgical approach after haemodynamic support using Impella.
    Case description: A 58-year-old man with type 2 diabetes mellitus and hypertension presented with three days of chest pain. Testing revealed late presenting acute anterior ischaemic infarction and left-to-right shunt in the apical ventricular septum. Urgent cardiac catheterisation showed near-total occlusion of the left anterior descending artery. An Impella CP® was placed before angioplasty with a drug-eluting stent to optimise haemodynamics. After a multidisciplinary discussion, the Impella CP® was upgraded to Impella 5.5®, and surgery was delayed allowing for scar formation. The patient remained in the intensive care unit, where he underwent physical therapy, showing improvements in exercise tolerance by the time of surgery. He underwent a left ventriculotomy with a successful repair via an endocardial patch 28 days after initial presentation. Post-operative recovery was uneventful, with the patient discharged five days later, reporting no physical limitations one month post-discharge.
    Conclusion: The successful management of VSD post-MI relies on interdisciplinary collaboration, careful timing of surgical intervention and the strategic use of mechanical support devices such as the Impella. This case highlights the potential for favourable outcomes when tailored treatment approaches are employed.

  • Geeta Bhagia, Nasir Hussain, Fnu Arty, Victor Farah, Robert Biederman
    Views: 152 HTML: 10 PDF: 97

    Background: Wellens’ syndrome is characterised by a history of chest pain with an abnormal electrocardiogram (EKG), demonstrating biphasic or deeply inverted T waves in leads V2–3 (may extend to involve all precordial and lateral limb leads – the type B Wellens’ pattern). A Wellens’ EKG pattern is considered highly specific for critical stenosis involving the ostial/proximal left anterior descending artery (LAD). However, there are no reported cases of an association of a Wellens’ EKG pattern with myopericarditis. Here, we present such a rare case.
    Case description: A thirty-one-year-old female with known essential hypertension and psoriatic arthritis presented with a constant, central chest pain radiating to the shoulders and back. The patient’s physical examination was unremarkable at presentation other than elevated blood pressure at 170/68 mmHg. An EKG at presentation demonstrated deep symmetric T-wave inversions in anterolateral leads with elevated high-sensitivity troponin, and an elevated erythrocyte sedimentation rate. The patient was referred to the cardiac catheterisation laboratory for concerns of a Wellens’ EKG pattern; however, invasive angiography demonstrated only obtuse marginal branch disease – no LAD disease was noted. Cardiac magnetic resonance (CMR) imaging confirmed the diagnosis of myopericarditis and absence of myocardial infarction. The patient was medically managed and discharged home in a stable condition.
    Conclusion: In literature and established clinical practice, the Wellens’ EKG pattern is considered highly concerning for critical ostial/proximal LAD stenosis. However, we now propose that myopericarditis may be considered in a differential diagnosis for this EKG pattern.

  • Muhammad Azhar Rosyidi, Valerinna Yogibuana, Ardian Rizal
    Views: 156 HTML: 10 PDF: 91

    Syncope is a brief loss of consciousness caused by reduced blood flow to the brain, characterised by sudden onset, short duration and full recovery without intervention. Anamnesis, physical examination and other diagnostic tests such as laboratory analysis and electrocardiogram (ECG) can be conducted to identify the underlying cause of syncope. A Brugada pattern on an ECG in individuals with syndrome of inappropriate antidiuretic hormone secretion (SIADH) who have syncope symptoms may indicate cardiac issues. A 69-year-old man with hypertension and a history of smoking presented with syncope. His vital signs were within normal limits, with no signs of a neurological deficit. The patient met the diagnostic criteria for SIADH, as evidenced by the presence of hyponatraemia (Na 118 mmol/l), a hyperosmolar condition and euvolemia. Upon arrival, a twelve-lead ECG showed ST-segment anomalies that reflected a Brugada ECG pattern. No ventricular arrhythmias were detected during the 24-hour Holter monitoring. Coronary angiography revealed no abnormalities in the coronary arteries. The ECG demonstrated the normalisation of ST elevations and the disappearance of the Brugada ECG pattern after the correction of hyponatraemia. After three months of follow-up the patient, with a normal sodium level, had no episodes of syncope.

  • Fares Saliba, Jonathan Mina, Laurence Aoun, Georges Khattar, Elie Bou Sanayeh , Omar Mourad, Saif Abu Baker
    Views: 185 HTML: 16 PDF: 142

    Background: Cardiac sarcoidosis can cause a wide range of symptoms, including shortness of breath, chest pain, oedema, and fatal arrhythmias such as ventricular tachycardia (VT). Because the symptoms can be nonspecific, diagnosing cardiac sarcoidosis can be challenging. Treatment options may include corticosteroids to reduce inflammation, immunosuppressive drugs to prevent further damage, medications to control symptoms, ablation procedures, and defibrillators to prevent cardiac arrest.
    Case: A 60-year-old woman who has sarcoidosis affecting multiple organs including cardiac sarcoidosis, non-ischemic cardiomyopathy with reduced ejection fraction, and hypertension, was admitted with tachycardia, shortness of breath, and a recently fired automatic implantable cardioverter defibrillator (AICD). Three months prior, the patient was admitted for a syncopal episode and diagnosed with cardiac sarcoidosis through cardiac magnetic resonance imaging (MRI) and positron emission tomography (PET), which demonstrated active inflammation, and an AICD was implanted. During this admission, the patient had an episode of ventricular tachycardia and was treated with amiodarone and lidocaine. The patient received steroids, sacubitril/valsartan, and methotrexate. After 48 hours of observation, the patient was discharged without further events.
    Conclusion: Cardiac sarcoidosis is a rare but serious disease that can lead to life-threatening cardiac complications such as ventricular tachycardia. Early diagnosis and aggressive management are crucial for improving outcomes and preventing sudden cardiac death. AICD implantation as a secondary prevention in cardiac sarcoidosis might prevent cardiac arrest.

  • Fares Saliba, Jonathan Mina, Laurence Aoun, Georges Khattar, Elie Bou Sanayeh, Jennifer Jdaidani, Ibrahim Al Saidi
    Views: 248 HTML: 87 PDF: 225

    Background: Studies have shown major cardiovascular effects associated with ketamine use disorder including dose-dependent negative inotropic effects. Preoperative ketamine use has been linked to ketamine-induced stress cardiomyopathy.
    Case presentation: A 28-year-old female with a history of recurrent cystitis and ketamine use disorder (twice weekly for 14 years) presented with bilateral lower extremity oedema and shortness of breath for 3 months. She was tachycardic with a troponin level of 0.07 ng/ml and a B-type natriuretic peptide (BNP) level of 2511 pg/ml. Electrocardiogram showed normal sinus rhythm and transthoracic echocardiography (TTE) showed left ventricular ejection fraction (EF) of 15%, dilated left ventricle, and severe tricuspid and mitral regurgitation. Computed tomography (CT) scan of the chest and abdomen showed bilateral pleural effusions with congestive hepatopathy and ascites. The patient was started on intravenous furosemide, metoprolol, and sacubitril/valsartan. Rheumatological workup including complement levels, and antinuclear anti-double-stranded DNA was negative. A repeat TTE 2 weeks later revealed an EF of 25% and moderate tricuspid regurgitation. Four months later, the EF was 54% with normal left ventricular cavity size.
    Conclusion: Although ketamine use disorder is increasing, data on long-term side effects is minimal. Screening for ketamine use disorders should be considered in patients presenting with acute systolic heart failure. Long-term studies are needed to evaluate the benefits of adding ketamine screening to standard urine toxicology.

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