Simultaneous right coronary artery spasm in a patient with Anterior ST-Segment Elevation Myocardial Infarction: a case report

Please cite this article as: Taherpour Z, Seyedian M, Alasti M. Simultaneous right coronary artery spasm in a patient with Anterior ST-Segment Elevation Myocardial Infarction: a case report. Novel Biomed 2013;1:29-33.Simultaneous occlusion of two vessels causing infarction at different territories is an uncommon finding. We report simultaneous right ventricular and anterior ST-segment elevation myocardial infarction in a previously healthy young man.The angiographic results demonstrated the simultaneous occlusion of the right and left coronary arteries because of simultaneous occlusion of left anterior descending artery (LADA) and spasm of right coronary artery (RCA). In this patient, we found simultaneous ST elevations in right and precordial leads so everyone should be careful about all leads of the surface electrocardiogram for decision making in the management of a patient

Infra-His Block in a Normal Heart

A 55 year old man with history of palpitation was referred for electrophysiologic study. Baseline ECG, physical examination and transthoracic echocardiographic study were normal. Electrophysiologic study revealed normal AH and HV intervals. Pacing of right atrium with a cycle length of 300 msec showed 2:1 AV block. AH interval was 252 msec and the block was infra-his (Figure 1). With continual of right atrial pacing, one to one AV conduction with increasing AH interval to 282 msec and QRS widening (LBBB pattern) were being observed. HV intervals during 2:1 block and during 1:1 AV conduction were normal. What is the mechanism? Is it an abnormal finding in this patient

Concealed Malfunction of The Temporary Pacemaker

The 12-lead ECG shows sequential atrial and ventricular pacing (Figure 1A). A tracing, obtained simultaneously during pacemaker interrogation, disclosed pacemaker functioning as VDD mode (Figure 1B). The careful examination of this pacemaker tracing showed that there is a pacing stimulus before each P wave (compatible with DDD mode). This paradox can only be explained by displacement of the temporary pacing lead to right atrium and right atrial stimulation by temporary pacemaker. In this setting, each temporary pacemaker-induced atrial depolarization is tracked by the right atrial lead of the permanent pacemaker as intrinsic P wave. Fluoroscopic study confirmed this explanation (Figure 2). The displaced temporary pacing lead was seen near the lateral right atrial wall. Temporary pacemaker lead had been inserted before replacement of permanent pacemaker

Shortening of ventriculoatrial interval after ablation of an accessory pathway

A 21-year old man with history of 8 year palpitation was referred for electrophysiologic study and possible radiofrequency ablation. Physical examination and transthoracic echocardiographic study did not disclose any abnormality. Baseline ECG showed normal sinus rhythm with normal PR and QRS intervals and no evidence of preexcitation. Antiarrhythmic drugs (propranolol and verapamil) were discontinued two days before the procedure. Baseline intervals in sinus rhythm were as follows: sinus cycle length=690 msec, AH=74 msec, HV=37 msec, QRS=90 msec, PR=133 msec. The minimal pacing cycle length maintaining 1:1 antegrade conduction (AVWP) was 320 msec and the minimal pacing cycle length maintaining 1:1 retrograde conduction (VAWP) was 400 msec. Single extrastimulus testing in the right atrium and the right ventricular apex leaded to a sustained narrow complex tachycardia. The arrhythmia was a short PR- long RP tachycardia with following characteristics: cycle length=376 msec, AH=141 msec, HV=42 msec, VA=200 msec, HA (HRA) =236 msec, HA (His) =243 msec and eccentric atrial activation during the arrhythmia (Figure 1). The arrhythmia was easily reproducible with stable hemodynamic

Predictors of appropriate ICD therapy in patients with implantable cardioverter-defibrillator

BACKGROUND: Understanding the predictors of appropriate implantable cardioverter defibrillator (ICD) therapy could help to better identify candidates for ICD implantation. METHODS: One hundred and sixty two patients with ICD (111 with coronary artery disease [CAD] and 51 with dilated cardiomyopathy [DCM]) were included in the study. Clinical, electrocardiographic, and ICD stored data and electrograms were collected. RESULTS: During mean follow up of 15±11 months 54 patients (33%) received ≥ 1 appropriate ICD therapy (AICDT). We used binary logistic regression analysis with forward selection method to find the potential predictors of appropriate ICD therapy after device implantation. Male gender (odds ratio [OR] = 2.76, 95% confidence interval [CI] = 1.1 – 7.1, P=0.021), DCM as underlying heart disease (OR = 4.2, 95% CI = 1.9 – 9.5, P=0.001), and QRS width > 100 ms (OR = 2.58, 95% CI = 1.2 – 5.4, P=0.010) were correlated with increased likelihood of AICDT during the follow up period. In subgroup analysis of the patients with CAD and DCM, QRS duration > 100 ms was correlated with the probability of ≥ 1 AICDT. In our patients indication of ICD implantation (primary versus secondary prevention) did not influence probability of ≥ 1 AICDT (adjusted OR = 1.66, 95% CI = 0.7 – 4.0, Mantel-Haenszel P value P=0.355.) CONCLUSION: QRS width could be used as an additional simple risk stratifier beyond EF to identify potential candidates who would benefit more from ICD implantation. This may have practical implications for patient selection especially in developing countries. Indication of ICD implantation (primary versus secondary prevention) did not affect the probability of ≥ 1 AICDT during the follow up period

Mutation analysis of connexin 26 gene and del (GJB6-D13S1830) in patients with hereditary deafness from two provinces in Iran

Mutations in the connexin 26 (Cx26) gene at the DFNB1 locus on chromosome 13q12 are associated with autosomal recessive non-syndromic hearing loss (ARNSHL). There are many known mutations in this gene that cause hearing loss. A single frameshift, at position 35 (35delG) accounts for 50% of mutations in the Caucasian population with carrier frequencies of 1.5-2.5%. In this study we investigated the prevalence of Cx26 gene mutations by directly sequencing the coding exon of this gene belonging to ARNSHL individuals from 53 families in Qom and Markazi provinces of Iran. Seven different Cx26 variants were identified. Five Cx26 mutations including 35delG, 233delC, 176del16, W24X, L90P were found in 10 of 53 families (18.87%). One olymorphism V153I was also found. One variant A171T with unknown effects was also detected. Six of the 53 families were observed to have GJB2 mutations in both alleles (11.32%). The most common mutation was 35delG. Three out of 10 families (30%) with GJB2 variants contained 35delG mutation in both alleles and the frequency of 35delG allele was 0.50 among 10 out of 53 families. Also screening for the 342-kb GJB6 deletion mutant did not reveal any large deletion among families studied. Thus, in the two provinces, contribution of GJB2 (Gap Junction Protein Beta 2) mutations to familial deafness appears to be less significant. This necessitates further assessment of the other known genes regions as well as a search for new genetic factors in hereditary deafness in the Iranian population

Contribution of GJB2 mutations and Four common DFNB loci in autosomal recessive non-syndromic hearing impairment in Markazi and Qom provinces of Iran

This study aimed to investigate the contribution of four common DFNB ("DFN" for deafness and "B" for autosomal resessive locus) loci and GJB2 gene mutations (exon 2) in hearing impairment in individuals living in Markazi and Qom provinces of Iran. Forty consanguineous Iranian families with at least three affected individuals in family or pedigree who suffer from an autosomal recessive non-syndromic congenital hearing impairment were the subjects of this study. Blood samples were taken from both hearing and non-hearing individuals, DNA was extracted and amplified by using specific primers for the coding region of GJB2 gene (exon 2). The PCR product of GJB2 gene was then sequenced. Also short tandem repeat (STR) markers amplified by using specific primers for loci DFNB2, DFNB3, DFNB4 and DFNB21. At least 2 microsatellite markers (STR) for each DFNB locus exceeding to 4-6 markers for the linked families were used. The amplified markers were analyzed by conventional Polyacrylamide Gel Electrophoresis followed by silver staining. Six families were homozygous or compound heterozygous for GJB2 mutations and were excluded from further studies. Linkage analysis was carried out for the remaining 34 families by genotyping the flanked STR markers of DFNB2, DFNB3, DFNB4 and DFNB21 loci. Six families showed linkage; including one family to DFNB2, two families to DFNB3 and three families to DFNB4 locus while no family showed linkage to DFNB21 locus. Undoubtedly, the best understanding of the genetic basis of hearing loss in Iranian population will be achieved by performing similar experiments in other provinces and also by analyzing more loci

Genetic Linkage Analysis of 15 DFNB Loci in a Group of Iranian Families with Autosomal Recessive Hearing Loss

Background: Hearing loss (HL) is the most frequent sensory birth defect in humans. Autosomal recessive non-syndromic HL (ARNSHL) is the most common type of hereditary HL. It is extremely heterogeneous and over 70 loci (known as DFNB) have been identified. This study was launched to determine the relative contribution of more frequent loci in a cohort of ARNSHL families. Methods: Thirty-seven Iranian families including 36 ARNSHL families and 1 family with Pendred syndrome each with >= 4 affected individuals, from seven provinces of Iran, were ascertained. DFNB1 contribution was initially studied by DNA sequencing of GJB2 and linkage analysis using the relative STR markers. The excluded families were then subjected to homozygosity mapping for fifteen ARNSHL loci. Results: Sixteen families were found to be linked to seven different known loci, including DFNB I (6 families), DFNB4 (3 families +1 family with Pendred syndrome), DFNB63 (2 families), DFNB2 (1 family), DFNB7/11 (1 family), DFNB9 (1 family) and DFNB21 (1 family). DNA sequencing of the corresponding genes is in progress to identify the pathogenic mutations. Conclusion: The genetic causes were clarified in 43.2% of the studied families, giving an overview of the causes of ARNSHL in Iran. DFNB4 is ranked second after DFNB1 in the studied cohort. More genetic and epigenetic investigations will have to be done to reveal the causes in the remaining families