Moustafa Elsheshtawy

Synthetic Marijuana Induced Acute Nonischemic Left Ventricular Dysfunction

Synthetic marijuana is an uptrending designer drug currently widely spread in the US. We report a case of acute deterioration of nonischemic left ventricular dysfunction after exposure to synthetic marijuana. This case illustrates the importance of history taking in cardiac patients and identifies a negative cardiovascular effect of synthetic marijuana known as K2, not yet well detected by urine toxicology screening tools.

Left ventricular aneurysms in hypertrophic cardiomyopathy with midventricular obstruction: A systematic review of literature

Hypertrophic cardiomyopathy (HCM) with or without left ventricular apical aneurysm (LVA) had been studied in the past. Midventricular obstruction associated with HCM and LVA is a unique entity that has not been distinguished previously as a separate phenotypic disease in HCM patients.

Anomalous muscular bands of the left atrium on echocardiography

A 22-year old male, with a history of hypertension, myocarditis and cellulitis, was hospitalized with Streptococcus Dysglactiae septicemia. An echodense structure was noted on apical 4-chamber view by transthoracic echocardiogram (TTE) (Fig. 1 a, b), stretching between the ridge of the left atrial appendage and the atrial septum consistent with an anomalous muscular band (AMB). Case 2: A 56-year-old male, with no significant history, was hospitalized with cryptogenic ischemic stroke. TTE revealed a patent foramen ovale (PFO) with a significant moderate right-to-left shunt. Prior to a transcatheter closure, surgeon’s view by 3D transesophageal echocardiogram (TEE) (Fig. 1c) demonstrated the peculiar attachment of an AMB from the posterior annulus to the A2 scallop leading to a bridge type double orifice mitral valve (DOMV).

Congenital inferior sinus venosus defect associated with pulmonary valve stenosis: A late presentation of a rare disease

Congenital inferior sinus venosus defect (SVD) is a rare congenital heart disease. Proper diagnosis of this disease is challenging and requires understanding of cardiac hemodynamics. Here, we discuss a patient with a late presentation of combined congenital inferior SVD associated with congenital pulmonary stenosis.

A Case of Hyperacute Severe Thrombocytopenia Occurring Less than 24 Hours after Intravenous Tirofiban Infusion

Thrombocytopenia is defined as a condition where the platelet count is below the lower limit of normal (<150 G/L), and it is categorized as mild (100–149 G/L), moderate (50–99 G/L), and severe (<50 G/L). We present here a 79-year-old man who developed severe thrombocytopenia with a platelet count of 6 G/L, less than 24 hours after intravenous tirofiban infusion that was given to the patient during a percutaneous transluminal coronary angioplasty procedure with placement of 3 drug-eluting stents. The patients baseline platelet count was 233 G/L before the procedure. Based on the timeline of events during hospitalization and laboratory evidence, it was highly likely that the patients thrombocytopenia was the result of tirofiban-induced immune thrombocytopenia, a type of drug-induced immune thrombocytopenia (DITP) which occurs due to drug-dependent antibody-mediated platelet destruction. Anticoagulant-mediated artefactual pseudothrombocytopenia was ruled out as no platelet clumping was seen on the peripheral blood smears. The treatment of DITP includes discontinuation of the causative drug; monitoring of platelet count recovery; or treatment of severe thrombocytopenia with glucocorticoids, IVIG, or platelet transfusions depending on the clinical presentation. The most likely causative agent of this patients thrombocytopenia—tirofiban—was discontinued, and the patient did not develop any signs of bleeding during the remainder of his hospital stay. His platelet count gradually improved to 24 G/L, and he was discharged on the sixth hospital day.

Primary cardiac angiosarcoma. Histopathology imaging correlation

We report a novel observation of a cardiac hemangioma possible transformation into cardiac angiosarcoma. This report should give a new insight on the pathogenesis of the tumor, always thought to have a de-novo genesis. We emphasize in our report the value of combining imaging modalities to examine the anatomic and metabolic properties of cardiac tumors providing a valuable tool for comprehensive assessment. <Learning objective: Assessment of cardiac tumors should combine different imaging modalities to examine the anatomic and metabolic properties of the lesions. We report a novel observation on cardiac angiosarcoma possible transformation from a cardiac hemangioma. This report should give a new insight into the pathogenesis of the tumor, always thought to have a de-novo genesis.>.

Hypothyroidism and congenital long QT: Additive effect causing torsades

A 19-year-old woman was hospitalized following a syncope episode. Initial investigations in the emergency department revealed thyroid-stimulating hormone (TSH; 679 m/mL; normal 0.35–5.5 m/mL), free thyroxine (T4; 0.36 ng/dL; normal 0.93–1.7 ng/dL), triiodothyronine (T3; 23.53 ng/dL; normal 84–202 ng/dL), calcium (9.8 mg/dL), potassium (K; 3.7 mmol/L), and negative urine toxicology. Corrected QT interval (QTc) was noted to be 523 ms on admission electrocardiography, and the patient was consequently started on intravenous hydrocortisone and synthroid therapy. During the first day of hospitalization, patient had pre-syncope with corresponding telemetry strip showing torsades de pointes (Figure 1). Patient was given 2 g of intravenous magnesium sulfate and transferred to the coronary care unit. Echocardiography revealed preserved left ventricular ejection fraction. QTc improved to 329 ms after regaining euthyroid status with corresponding TSH 0.3 (m/mL), and the decision to place an implantable cardioverter–defibrillator (ICD) was deferred. The patient was later tested for a congenital long QT syndrome in a panel of 30 genes accounting for most of the arrhythmic hereditary diseases. Genetic testing revealed heterozygosity for a novel frameshift mutation c.2470delG in KCNH2 (HERG) gene. Although the c2470delG mutation in the KCNH2 gene has not been reported to our knowledge, this mutation causes a shift in the reading frame starting at codon alanine 824, changing it to a proline, and creating a premature stop codon at Position 44 of the new reading frame, denoted p.Ala824ProfsX44. This mutation is expected to result in either an abnormal truncated protein product or a loss of protein from this allele through non-sense-mediated messenger RNA decay. The patient was also heterozygous for a published variant of unknown significance in the GPD1L gene. Serum TSH correlates with cardiovascular changes and risk of potentially life-threatening arrhythmias in hypothyroid patients. Modulation of K channels function by low circulating T3 leads to a disproportionate lengthening of the action potential and consequent lengthening of QT interval. Ventricular arrhythmias are usually reversible with levothyroxine replacement therapy, unwarranting ICD placement following acute-phase resolution.