The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology最新文献

Background: Hypertrophic cardiomyopathy (HCM) is a prevalent hereditary cardiac disorder characterized by marked myocardial hypertrophy, which may lead to impaired diastolic function and relative myocardial ischemia. On rare occasions, HCM coexists with coronary artery disease (CAD), complicating therapeutic decisions due to heightened risks of heart failure and ischemic events. Treatment options for these patients commonly include surgical myomectomy or alcohol septal ablation, traditionally performed using an over-the-wire (OTW) balloon catheter. Here, we present a case in which a modified 'block and delivery' alcohol septal ablation technique was utilized, instead of the conventional OTW approach, in a patient with concurrent HCM and CAD within a resource-limited setting.

Case presentation: A 40-year-old Asian female presented with angina and acute heart failure in our clinic. Diagnostic evaluations revealed hypertrophic obstructive cardiomyopathy (HOCM) with severe left ventricular outflow tract obstruction (LVOTO) and significant coronary artery stenosis. Due to equipment constraints, the patient underwent staged interventions: a percutaneous coronary intervention (PCI) followed by alcohol septal ablation using a modified technique. This intervention effectively reduced the LVOT gradient from 108 to 17 mmHg. At the one-year follow-up, the patient demonstrated good health, complete symptom resolution, and a normal left ventricular outflow tract gradient.

Conclusion: This case illustrates the feasibility of employing a modified alcohol septal ablation technique in resource-limited settings, highlighting the importance of adaptable and innovative approaches in managing complex cardiac conditions.

Background: Ischemic cardiomyopathy is a condition that represents myocardial dysfunction due to obstructive coronary artery disease. In ischemic cardiomyopathy, both structural and electrical remodeling occur. Myocardial biomarker, soluble ST2 (sST2) is able to predict patient's mortality and morbidity, and structural remodeling of the heart is responsible for its expression. ECG dispersion mapping (ECG-DM) as evaluated by myocardial micro-alternation index (MMI) may predict alteration of the myocardial electrophysiology with high sensitivity and specificity. The association between structural and electrical remodeling in ischemic cardiomyopathy is not fully understood. This study aims to evaluate the correlation between MMI and sST2 level in patients with ischemic cardiomyopathy.

Result: Total patients who met for the inclusion criteria were 30 patients. Mean age was 57.97 ± 10.04 years; most patients were male (80%). 27 (90%) patients had class II NYHA functional class. The most common risk factors were smoking (20 (66,7%)) and hypertension (17 (56,7%)). Median MMI was 34.0% (IQR: 23.0-42.3%) and median sST2 was 5.6 ng/mL (IQR: 2.0-11.5 ng/mL). This study found that MMI had a significant correlation with sST2, indicating a link between structural and electrical remodeling in ischemic cardiomyopathy (r = 0.583, p < 0,05).

Conclusion: There was a correlation between MMI and sST2 in patients with ischemic cardiomyopathy.

Background: Transcatheter stenting has become the preferred treatment for native and recurrent coarctation of aorta (CoA), but complications such as stent migration occur in approximately 5% of cases. Proximal stent migration is particularly challenging and often requires surgical intervention. This report highlights the successful transcatheter management of proximal stent migration during CoA stenting in a high-risk patient.

Case presentation: A 22-year-old woman with Turner syndrome and chronic idiopathic thrombocytopenia purpura (ITP) presented with severe native CoA and refractory hypertension. Echocardiography revealed severe left ventricular hypertrophy and bicuspid aortic valve with mild aortic stenosis. The CoA segment gradient was 90 mmHg. During stent implantation using a 16 × 44 mm Zephyr stent mounted on an Atlas balloon, the stent migrated proximally into the right brachiocephalic artery despite appropriate crimping and hypotensive pacing. The stent was stabilized using a pigtail catheter via the right radial artery, and a low-profile peripheral balloon was inflated distal to the stent to pull the system back. However, the stent became stuck at the tightest segment of the CoA. Predilation of the CoA site with a larger balloon widened the segment, allowing the stent to be repositioned and deployed successfully. Post-procedure, the gradient across the CoA decreased to less than 5 mmHg. The patient was discharged after two days without complications, and follow-up imaging confirmed proper stent placement without restenosis.

Conclusions: Our case illustrates the transcatheter management of proximal stent migration during CoA stenting, potentially reducing the need for surgical intervention. A stepwise strategy involving stent stabilization, low-profile balloon-assisted repositioning, and predilation of tight CoA segments can facilitate successful stent repositioning. This case contributes to the existing literature by documenting the occurrence and management of this rare complication.

Background: Dilated cardiomyopathy (DCM) is a primary myocardial disease characterized by systolic dysfunction, which can lead to disparity and disorganized contraction, commonly referred to as dyssynchrony. Three types of dyssynchrony include atrioventricular (AVD), interventricular (inter-VD), and intra-LV dyssynchrony (intra-VD). We aimed to investigate the prevalence and interdependence of electrical and mechanical dyssynchrony in order to elucidate the optimizing patients for cardiac resynchronization therapy (CRT).

Results: A total of 37 DCM patients (1-17 years, 51% female) were included in this cross-sectional study. Regarding the intra-VD, inter-VD, and AVD, the study showed inter-VD in 37%, 27%, and 48% by Doppler, Doppler tissue imaging (DTI), and color-coded DTI methods, respectively; however, 70% showed right ventricular free wall delay based on the presence of peak of strain after pulmonic valve closure. 86.5% (32/37) of patients show intra-VD. 100% (8/8) of DCM patients with prolonged QRS (QRSc ≥ 120 ms) had intra-VD, of which 12.5% (1/8) had mild, 25% (2/8) mod, and 62.5% (5/8) severe dyssynchrony. However, 82% (24/29) of patients with narrow QRS (QRSc < 120 ms) also had intra-VD, of which 17% (3/24) were mild, 62.5% (15/24) mod, and 25% (6/24) severe. There were 57% (21/37) of patients with AVD. 77% (10/13) of DCM patients with prolonged PRc (PR ≥ 200 ms) had AVD of which 31% (4/13) of patients had mild, 31% (4/13) mod, and 15% (2/13) severe AVD, while among PRc < 200 ms 46% (11/24) had AVD, of which 37.5% (9/24) had mild AVD, 4% (1/24) mod, and another 4% severe AVD. LVEF was lower and LV GLS, mortality, Pro-BNP, NYHA FC, and severity of intra-VD were higher in the group with QRS ≥ 120 ms, and PR ≥ 200 ms. 27% of patients were expired during the year of study. There was a significant direct correlation between mortality rate, NYHA FC, and pro-BNP with the severity of intra-, inter-VD, and AVD. The most delayed horizontal segments were inferolateral, anterolateral, anterior, and anteroseptal sequentially, while the highest level of vertical dyssynchrony (base to apex) was observed in inferoseptal, inferolateral, and anteroseptal walls in order.

Conclusions: Our findings indicated that DCM causes both intra- and inter-VD, associated with QRS duration concerning severity, which also results in AVD that are correlated with PRc interval. Notably, a substantial proportion of patients with narrow QRSc also demonstrated intra-VD and inter-VD, while nearly half of those with normal PRc exhibited AVD. Collectively, these observations suggest a lack of complete correspondence between electrical and mechanical dyssynchrony.

Background: Injuries from lightning strikes are infrequent but potentially life-threatening, mainly caused by indirect electrical injuries. Although various organ systems can be involved, the effects of electric current on the cardiovascular system can manifest as electrocardiographic (ECG) changes, elevated cardiac-specific enzymes, and cardiac and respiratory arrest, although rare. This case report aims to describe the ECG changes that occur due to lightning strikes and resemble the features of non-ST elevation myocardial infarction (NSTEMI).

Case presentation: A 31-year-old man with no history of cardiovascular disease risk factors other than being an active smoker presented to the emergency department after being unconscious for 15 min due to a lightning strike while digging a grave. He complained of headache, tingling in the extremities, and general weakness. The physical examination found no burns or bruises. The initial ECG examination showed inferior ST depression with elevated troponin-I, which led to the diagnostic features of NSTEMI. When a repeat ECG examination was performed the next day, an inverted T wave was found in the inferior leads. Echocardiographic examination revealed only concentric left ventricular hypertrophy and mild diastolic dysfunction without kinetic abnormalities. Because it was assumed that the NSTEMI features were not due to an atherothrombotic process, the patient was treated conservatively without worsening his condition.

Conclusions: Lightning strikes can cause a range of cardiac injuries, from mild ECG changes to fatal damage. Early recognition of lightning injury syndrome and close monitoring of complications through signs and symptoms, ECG, cardiac enzymes, and echocardiography are crucial for improving patient outcomes.

Background: Smoking, including conventional and electronic cigarettes (e-cigarettes), is a major contributor to cardiovascular morbidity and mortality. Indonesia, with 69.1 million smokers, experiences a high burden of smoking-related diseases. This study aims to evaluate the impact of conventional and e-cigarette exposure on atherosclerosis in Rattus norvegicus (Wistar rats).

Methods: Twenty-one male Wistar rats were randomized into three groups: control, conventional cigarette exposure, and e-cigarette exposure. Both smoking groups received equivalent nicotine doses for 30 min daily, five days a week, for 12 weeks. Aortic and iliac artery intima-media thickness (IMT) was measured, and plasma levels of tumor necrosis factor-alpha (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) were analyzed using ELISA. Histopathological changes were also examined.

Results: Cigarette exposure significantly increased IMT in the aorta (control: 67.22 ± 3.07 µm; conventional: 100.89 ± 25.60 µm; e-cigarette: 83.75 ± 7.45 µm; p < 0.05) and iliac arteries (control: 68.50 ± 5.6 µm; conventional: 90.49 ± 25.02 µm; e-cigarette: 90.68 ± 12.26 µm; p = 0.031). MCP-1 levels were significantly elevated in the conventional group (205.77 ± 22.18 pg/mL; p = 0.003), while TNF-α levels increased in both groups but without statistical significance. Histopathology revealed fatty streaks and elastic fiber disruption in both exposure groups, with no significant differences observed (p > 0.05).

Conclusions: Both conventional and e-cigarettes promote atherosclerosis, as evidenced by increased arterial thickness and inflammatory markers. The cardiovascular risks associated with e-cigarettes are comparable to those of conventional cigarettes, highlighting the need for stricter regulation and public awareness.

Background: Extracorporeal membrane oxygenation (ECMO), which provides life-saving assistance in severe cardiac and pulmonary failure cases, has emerged as an important technique in managing children with congenital heart disease (CHD).

Main body: In this review, we discuss the evolution of ECMO over the years, its clinical uses, and the results in pediatric CHD. ECMO has been utilized as a bridge to recovery, in stabilizing an individual after surgery, and as a bridge to heart transplantation. Cannulation procedures that are adjusted according to the anatomy of an individual have improved outcomes, although bleeding and neurologic concerns remain a matter of concern. In addition, long-term neurodevelopmental disorders and renal failure are also among the alarming outcomes. The use of newer anticoagulant drugs like bivalirudin, which lowers the risk of bleeding, and genomic testing for personalized treatment are examples of recent developments. Furthermore, neuroprotective techniques such as erythropoietin and dexmedetomidine can also enhance the neurocognitive outcomes. Finally, improvements in monitoring systems and pump technology contribute to increased ECMO efficacy and safety.

Conclusion: Despite these developments, ECMO's expense and restricted accessibility remain major obstacles, especially in areas with low resources. In this review, the advancements in ECMO technology and care are highlighted, and it also emphasizes future research to address the current challenges.

Background: Amiodarone is an antiarrhythmic drug known for its potential side effects, one of which is neuromyopathy, though it remains relatively rare. This condition can present with muscle weakness, pain, and tremors, potentially leading to functional impairment. The exact mechanisms underlying amiodarone-induced neuromyopathy are not fully understood but may involve both direct muscle toxicity and effects on nerve conduction.

Case presentation: We present the case of a 68-year-old man with symptomatic arrhythmogenic right ventricular dysplasia, receiving long-term amiodarone, experiencing bilateral leg pain and weakness associated with amiodarone use. On clinical examination, motor strength in the lower limbs was rated at 2/5, with decreased tactile sensation. The biological assessment showed normal level of creatine kinase and C-reactive protein. The spinal MRI was normal. Electromyography "EMG" revealed a non-length dependent sensorimotor demyelinating polyneuropathy. After discontinuing amiodarone, both mobility and function showed significant improvement.

Conclusion: These observations highlight the importance of performing neurologic examinations in patients treated with amiodarone to identify even rare complications, such as neuromyopathy. Importantly, neuromyopathy is often reversible following discontinuation of the drug.

Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2is) show promise as a therapy for heart failure (HF); however, the safety and efficacy of SGLT2i in different HF etiologies are uncertain, thus arising the need for a meta-analyses.

Main text: PubMed and Scopus were queried until May 2023 for studies comparing SGLT2i with placebo in HF patients with ischemic and non-ischemic etiologies. Meta-analyses were performed using risk ratio and hazard ratio. A fixed effect model was used. Outcomes assessed were hospitalization due to HF (HHF), cardiovascular death (CVD), CVD/HHF, all-cause mortality, volume depletion, fracture, and discontinuation of drug due to adverse effects. Four RCTs were included (15,676 patients). Analysis revealed no significant differences in CVD/HHF between ischemic [HR: 0.77 (0.70-0.86) P < 0.00001] and non-ischemic patients [HR: 0.72 (0.65-0.80) P < 0.00001] using SGLT2i (P = 0.35). Significant reductions were seen in HHF in both ischemic [RR 0.74 (0.65-0.84) P < 0.00001] and non-ischemic [RR 0.68 (0.59-0.78) P < 0.00001] patients (P = 0.39), with the effect more notable in the non-ischemic cohort. However, CVD significantly decreased in non-ischemic patients [RR 0.78 (0.63-0.95) P = 0.01], whereas no significant reduction was noted in ischemic patients [RR 0.94 (0.80-1.10) P = 0.43] (P-interaction = 0.15). All-cause mortality was significantly reduced in non-ischemic patients [RR 0.80 (0.67-0.96) P = 0.02] but not in ischemic patients [RR 0.96 (0.83-1.10) P = 0.52]. No significant safety events were observed in the SGLT2i cohort including volume depletion [RR 1.08 (0.94-1.25) P = 0.26], fracture [RR 1.02 (0.77-1.36) P = 0.88], or discontinuation of drug due to adverse effects [RR 0.97 (0.86-1.10) P = 0.65].

Conclusion: Similar CVD/HHF outcomes for ischemic and non-ischemic patients with SGLT2i. Significant HHF reductions in both groups. Non-ischemic patients showed greater improvements in CVD and all-cause mortality. However, no subgroup difference between ischemic and non-ischemic cause of heart failure was noted in our analysis.