Hypocalcemia – ABC CARDIOL

ABCIC

Case Report

Hypocalcemia and Reversible Cardiomyopathy Assessed by Magnetic Resonance Imaging

Bruno Lenzi et al. Gustavo Tortajada Victoria Rabaza Ernesto Cairoli Gabriel Parma

Introduction

Calcium is a fundamental component of biological systems and plays a key role in excitation-contraction coupling in cardiac myocytes. Calcium entry triggers a mechanism known as calcium-induced calcium release, in which calcium released from the sarcoplasmic reticulum is modulated by the influx of calcium from the extracellular space. Muscle contraction subsequently occurs through the interaction between calcium and the troponin-tropomyosin complex. In the heart, intracellular calcium is the primary regulator of contractile force (inotropism).

Hypocalcemia-induced cardiomyopathy is a rare condition with few reports in the scientific literature. We present a clinical case associated with hypoparathyroidism, one of the main causes of chronic hypocalcemia. This case report includes a novel element: the use of cardiac Magnetic Resonance Imaging (cMRI), which, to our knowledge, has not been previously described in the literature.

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ABC

Letter to the Editor

Suspension of Thiazide Diuretics in Advanced Chronic Kidney Disease. Time to Review an Old Concept

Rodrigo Bezerra et al. Flávio Teles de Farias Filho Audes Feitosa Wilson Nadruz … Andrea Araújo Brandão Weimar Kunz Sebba Barroso

The Hypertension Guidelines of the Sociedade Brasileira de Cardiologia (SBC), Brazilian Society of Hypertension (BSH), and Brazilian Society of Nephrology (BSN) recommend the use of loop diuretics to replace thiazides in patients with chronic kidney disease (CKD) stages 4 and 5, who have glomerular filtration rate (GFR) ≤ 30ml/min/1.73m².

These guidelines are in line with other guidelines, such as the European Hypertension Guideline (ESC/ESH 2018), which states that thiazide and thiazide-like diuretics are less effective in patients with GFR < 45ml/min/1.73m² and ineffective when GFR < 30ml/min/1.73m². However, the study that established this concept dates from 1961 and evaluated only 11 patients, among whom 5 had GFR < 37ml/min/1.73m². Despite this, this concept generated a dogma exported to textbooks, which has been propagated for decades as an incontestable truth.

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IJCS

Original Article

QTc, Tp-e Interval and Tp-e/QTc Ratio in Patients with Hypocalcemia-case Control Study

Begum Seyda Avci et al. Akkan Avci Arif Aksu Muge Gulen … Onder Yesiloglu Hasan Koca Salim Satar

Abstract

Background:

To the best of our knowledge, there are studies related to QT and QTc interval in patients with hypocalcemia, but there are no studies evaluating T wave peak and end interval (Tp-e interval), Tp-e/QT and Tp-e/QTc ratios used to evaluate cardiac arrhythmia risk and ventricular repolarization changes rates.

Objectives:

Therefore, we aimed to investigate whether there is a change in Tp-e interval, Tp-e/QT and Tp-e/QTc ratios in patients with hypocalcemia.

Methods:

Retrospectively, 29 patients with hypocalcemia in the emergency department were included in the study. Twenty-nine patients with similar age and sex distribution were included in the study as the control group. All patients underwent 12-lead electrocardiography (ECG). In addition to routine measurements, Tp-e interval, Tp-e/QT and Tp-e/QTc ratios were measured on ECG. The study data were grouped as patients with and without hypocalcemia.

Results:

The mean age of the patients was 66.24 ± 4.95 years. QTc interval, Tp-e interval and Tp-e/QTc values were found to be significantly higher in patients with hypocalcemia (p <0.001 for each). QTc interval, Tp-e interval and Tp-e/QTc ratio showed a significant negative correlation with calcium levels.

Conclusion:

Tp-e interval and Tp-e/QTc ratios are significantly increased in patients with hypocalcemia compared to those without hypocalcemia and this can be used more effectively in the follow-up of cardiac fatal arrhythmias.

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IJCS

Case Report

Cardiac Arrest Due to Hypocalcemia

Fernanda Aburesi Salvadori et al. Eduardo Martelli Moreira Murilo Bacchini Dias Amaro Nunes Duarte-Neto Edison Ferreira de Paiva

Discussion

Long QT syndrome (LQTS) can be congenital or acquired. The causes of acquired LQTS include hypocalcemia, due to prolongation of the phase 2 of the action potential (AP), medications (amiodarone, antidepressants and neuroleptics), hypokalemia, hypomagnesemia and severe bradycardia.^– LQTS is associated with a specific polymorphic ventricular tachycardia (VT), named as torsades de pointes (TdP), because of the characteristic shift in the QRS axis that gives the impression of a “torsion”.

The QT interval is a marker of the AP duration. In LQTS patients, the AP is prolonged unevenly across the myocardium, so as to cause high dispersion of repolarization. The AP prolongation favors the formation of early afterdepolarization (EAD), which are deformities in the plateau and rapid repolarization phases (2 and 3) capable of inducing ventricular extrasystoles. EADs in the unevenly repolarized myocardium are the cause of TdP. Tachycardia is sustained due to focal electric activity and/or a reentrant mechanism. It may either cease spontaneously or degenerate into ventricular fibrillation and cardiac arrest ^, .

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ABC

Original Article

Congenital Heart Disease as a Warning Sign for the Diagnosis of the 22q11.2 Deletion

Marcília S. Grassi et al. Cristina M. A. Jacob Leslie D. Kulikowski Antonio C. Pastorino … Roberta L. Dutra Nana Miura Marcelo B. Jatene Stephanie P. Pegler Chong A. Kim Magda Carneiro-Sampaio

Background:

To alert for the diagnosis of the 22q11.2 deletion syndrome (22q11.2DS) in patients with congenital heart disease (CHD).

Objective:

To describe the main CHDs, as well as phenotypic, metabolic and immunological findings in a series of 60 patients diagnosed with 22q11.2DS.

Methods:

The study included 60 patients with 22q11.2DS evaluated between 2007 and 2013 (M:F=1.3, age range 14 days to 20 years and 3 months) at a pediatric reference center for primary immunodeficiencies. The diagnosis was established by detection of the 22q11.2 microdeletion using FISH (n = 18) and/or MLPA (n = 42), in association with clinical and laboratory information. Associated CHDs, progression of phenotypic facial features, hypocalcemia and immunological changes were analyzed.

Results:

CHDs were detected in 77% of the patients and the most frequent type was tetralogy of Fallot (38.3%). Surgical correction of CHD was performed in 34 patients. Craniofacial dysmorphisms were detected in 41 patients: elongated face (60%) and/or elongated nose (53.3%), narrow palpebral fissure (50%), dysplastic, overfolded ears (48.3%), thin lips (41.6%), elongated fingers (38.3%) and short stature (36.6%). Hypocalcemia was detected in 64.2% and decreased parathyroid hormone (PTH) level in 25.9%. Decrease in total lymphocytes, CD4 and CD8 counts were present in 40%, 53.3% and 33.3%, respectively. Hypogammaglobulinemia was detected in one patient and decreased concentrations of immunoglobulin M (IgM) in two other patients.

Conclusion:

Suspicion for 22q11.2DS should be raised in all patients with CHD associated with hypocalcemia and/or facial dysmorphisms, considering that many of these changes may evolve with age. The 22q11.2 microdeletion should be confirmed by molecular testing in all patients.

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Hypocalcemia and Reversible Cardiomyopathy Assessed by Magnetic Resonance Imaging

Introduction

Suspension of Thiazide Diuretics in Advanced Chronic Kidney Disease. Time to Review an Old Concept

QTc, Tp-e Interval and Tp-e/QTc Ratio in Patients with Hypocalcemia-case Control Study

Abstract

Background:

Objectives:

Methods:

Results:

Conclusion:

Cardiac Arrest Due to Hypocalcemia

Discussion

Congenital Heart Disease as a Warning Sign for the Diagnosis of the 22q11.2 Deletion

Background:

Objective:

Methods:

Results:

Conclusion:

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