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1.
Neth Heart J ; 30(5): 282-288, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-34762282

RESUMO

BACKGROUND: Cryoballoon pulmonary vein isolation (PVI) is a common therapy for atrial fibrillation (AF). While moderately increased sinus rhythm heart rate (HR) after PVI has been observed, inappropriate sinus tachycardia (IST) is a rare phenomenon. We aimed to investigate the prevalence and natural history of an abnormal sinus HR response after cryoballoon PVI. METHODS: We included 169/646 (26.2%) patients with AF undergoing PVI with available Holter recordings before and 3, 6 and 12 months after the procedure. Patients with AF on Holter monitoring were excluded. Mean HR increase ≥ 20 bpm or an IST-like pattern (mean HR > 90 bpm or > 80 bpm when beta-blocking agents were used) following PVI was categorised as abnormal sinus HR response. RESULTS: Following PVI, mean HR ± standard deviation increased in the entire group from 63.5 ± 8.4 to 69.1 ± 9.9 bpm at 3 months (p < 0.001), and to 71.9 ± 9.4 bpm at 6 months (p < 0.001). At 12 months, mean HR was 71.2 ± 10.1 bpm (p < 0.001). Only 7/169 patients (4.1%) met criteria for abnormal sinus HR response: mean HR was 61.9 ± 10.6 bpm (pre-ablation), 84.6 ± 9.8 bpm (3 months), 80.1 ± 6.5 bpm (6 months) and 76.3 ± 10.1 bpm (12 months). Even at 12 months, mean HR was significantly different from that pre-ablation in this group (p = 0.033). However, in patients meeting IST-like pattern criteria, mean HR at 12 months was no longer significantly different from that pre-ablation. CONCLUSION: Few patients had an abnormal sinus HR response after PVI. Peak HR was observed 3 months after PVI, but HR was still significantly increased 12 months post-ablation compared with pre-ablation. An IST-like pattern was rarely observed. In these patients, HR decreased to pre-ablation values within a year.

2.
Neth Heart J ; 30(2): 84-95, 2022 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-34143416

RESUMO

BACKGROUND: The p.Arg14del (c.40_42delAGA) phospholamban (PLN) pathogenic variant is a founder mutation that causes dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM). Carriers are at increased risk of malignant ventricular arrhythmias and heart failure, which has been ascribed to cardiac fibrosis. Importantly, cardiac fibrosis appears to be an early feature of the disease, occurring in many presymptomatic carriers before the onset of overt disease. As with most monogenic cardiomyopathies, no evidence-based treatment is available for presymptomatic carriers. AIMS: The PHOspholamban RElated CArdiomyopathy intervention STudy (iPHORECAST) is designed to demonstrate that pre-emptive treatment of presymptomatic PLN p.Arg14del carriers using eplerenone, a mineralocorticoid receptor antagonist with established antifibrotic effects, can reduce disease progression and postpone the onset of overt disease. METHODS: iPHORECAST has a multicentre, prospective, randomised, open-label, blinded endpoint (PROBE) design. Presymptomatic PLN p.Arg14del carriers are randomised to receive either 50 mg eplerenone once daily or no treatment. The primary endpoint of the study is a multiparametric assessment of disease progression including cardiac magnetic resonance parameters (left and right ventricular volumes, systolic function and fibrosis), electrocardiographic parameters (QRS voltage, ventricular ectopy), signs and/or symptoms related to DCM and ACM, and cardiovascular death. The follow-up duration is set at 3 years. BASELINE RESULTS: A total of 84 presymptomatic PLN p.Arg14del carriers (n = 42 per group) were included. By design, at baseline, all participants were in New York Heart Association (NHYA) class I and had a left ventricular ejection fraction > 45% and < 2500 ventricular premature contractions during 24-hour Holter monitoring. There were no statistically significant differences between the two groups in any of the baseline characteristics. The study is currently well underway, with the last participants expected to finish in 2021. CONCLUSION: iPHORECAST is a multicentre, prospective randomised controlled trial designed to address whether pre-emptive treatment of PLN p.Arg14del carriers with eplerenone can prevent or delay the onset of cardiomyopathy. iPHORECAST has been registered in the clinicaltrials.gov-register (number: NCT01857856).

3.
Clin Genet ; 83(5): 452-6, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-22889254

RESUMO

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited myocardial disease that predominantly affects the right ventricle and is associated with ventricular arrhythmias that may lead to sudden cardiac death. Mutations within at least seven separate genes have been identified to cause ARVC, however a genetic culprit remains elusive in approximately 50% of cases. Although negative genetic testing may be secondary to pathogenic mutations within undiscovered genes, an alternative explanation may be the presence of large deletions or duplications involving known genes. These large copy number variants may not be detected with standard clinical genetic testing which is presently limited to direct DNA sequencing. We describe two cases of ARVC possessing large deletions involving plakophilin-2 (PKP2) identified with microarray analysis and/or multiplex ligation-dependent probe amplification (MLPA) that would have been classified as genotype negative with standard clinical genetic testing. A deletion of the entire coding region of PKP2 excluding exon 1 was identified in patient 1 and his son. In patient 2, MLPA analysis of PKP2 revealed deletion of the entire gene with subsequent microarray analysis demonstrating a de novo 7.9 Mb deletion of chromosome 12p12.1p11.1. These findings support screening for large copy number variants in clinically suspected ARVC cases without clear disease causing mutations following initial sequencing analysis.


Assuntos
Displasia Arritmogênica Ventricular Direita/genética , Deleção de Genes , Placofilinas/genética , Adulto , Displasia Arritmogênica Ventricular Direita/diagnóstico , Eletroencefalografia , Éxons , Ordem dos Genes , Humanos , Masculino , Mutação
4.
Ned Tijdschr Geneeskd ; 151(11): 627-9, 2007 Mar 17.
Artigo em Holandês | MEDLINE | ID: mdl-17441564

RESUMO

During the past decade, developments in the field of DNA diagnostics have resulted in the confirmation of the genetic nature of several cardiac diseases. In a cardiogenetics outpatient clinic, a cardiologist and a clinical geneticist together evaluate persons with a (possible) hereditary cardiac disease. It is of utmost importance that patients with hereditary cardiac diseases be recognised and subsequently referred for genetic counselling as several preventive and therapeutic options are available.


Assuntos
Cardiopatias/genética , Aconselhamento , Diagnóstico Precoce , Predisposição Genética para Doença , Testes Genéticos , Humanos
5.
Ned Tijdschr Geneeskd ; 150(18): 1027-31, 2006 May 06.
Artigo em Holandês | MEDLINE | ID: mdl-16715868

RESUMO

A 37-year-old man with symptomatic acute atrial fibrillation and a low-voltage electrocardiogram was treated with flecainide intravenously. Instead of conversion to sinus rhythm, he developed a wide-complex tachycardia suggestive of ventricular tachycardia. The patient recovered following electric cardioversion. First-choice therapy for symptomatic atrial fibrillation of recent onset (duration < 48 hours) is chemical conversion with a class IC antiarrhythmic drug (e.g. flecainide, propafenone). However, in patients with structural heart disorders, these drugs may induce ventricular tachycardia. A low-voltage electrocardiogram is suggestive of left ventricular damage. For these patients, electric cardioversion is a better alternative.


Assuntos
Antiarrítmicos/efeitos adversos , Flecainida/efeitos adversos , Taquicardia Ventricular/induzido quimicamente , Adulto , Antiarrítmicos/uso terapêutico , Fibrilação Atrial/tratamento farmacológico , Eletrocardiografia , Flecainida/uso terapêutico , Humanos , Masculino , Resultado do Tratamento , Função Ventricular/efeitos dos fármacos , Função Ventricular/fisiologia
6.
Am J Cardiol ; 70(11): 997-1003, 1992 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-1414918

RESUMO

The anti-ischemic efficacy of diltiazem may improve with increments in dosage and with additional beta-blocking therapy. However, the combined administration could lead to adverse effects through amplification of negative inotropic and chronotropic properties. To evaluate hemodynamic tolerability and safety of high-dose intravenous diltiazem in patients with coronary artery disease receiving long-term metoprolol treatment, 9 such patients were studied for 30 minutes after onset of intravenous diltiazem administration (0.5 mg/kg for 5 minutes, followed by 15 mg/hour). Diltiazem plasma levels peaked at 5 minutes (641 +/- 74 micrograms/liter), decreasing to 177 micrograms/liter at 30 minutes. Average metoprolol levels (43 +/- 12 micrograms/liter) did not change. Diltiazem immediately decreased systemic vascular resistance, left ventricular systolic and mean aortic pressures (29, 21 and 20%, respectively, at 5 minutes), and they remained significantly reduced at 30 minutes. Heart rate initially increased by 11% during the bolus infusion (p < 0.05). Concomitantly, contractility indexes Vmax and Vce40, measured at fixed heart rates, also increased significantly by 11%. Both heart rate and contractility indexes returned to baseline levels thereafter. Cardiac output increased by 10% (p = not significant), stroke index remained unchanged, but stroke work decreased significantly by 20%. Also, the tension-time index was significantly reduced (23%). Diltiazem induced moderate negative lusitropic effects, the first derivative of negative left ventricular pressure decline decreased by 12% and Tau 2 lengthened by 13%. Concomitantly, left ventricular filling pressure increased from 19 +/- 2 to 23 +/- 3 mm Hg, but only at 5 and 15 minutes. PQ, QRS and QTc intervals were not affected.(ABSTRACT TRUNCATED AT 250 WORDS)


Assuntos
Doença das Coronárias/tratamento farmacológico , Doença das Coronárias/fisiopatologia , Diltiazem/farmacologia , Sistema de Condução Cardíaco/efeitos dos fármacos , Hemodinâmica/efeitos dos fármacos , Metoprolol/uso terapêutico , Diltiazem/administração & dosagem , Interações Medicamentosas , Quimioterapia Combinada , Eletrocardiografia , Feminino , Humanos , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Função Ventricular Esquerda/efeitos dos fármacos
7.
Am J Cardiol ; 72(9): 647-51, 1993 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-8249838

RESUMO

Although a number of studies have shown that the incidence of late potentials is lower after thrombolytic therapy, it is not known whether this is paralleled by fewer arrhythmic events during long-term follow-up. In patients with first acute myocardial infarction, filtered QRS duration was significantly shorter when treated with streptokinase (95 +/- 11 ms, n = 53) than when treated with conventional therapy (99 +/- 12 ms, n = 77, p < 0.05). The low-amplitude signal (D40) was shorter after thrombolysis (28 +/- 11 vs 33 +/- 12 ms, p < 0.02). Terminal root-mean-square voltage did not differ significantly (41 +/- 24 vs 35 +/- 23 microV). Irrespective of treatment, late potentials were predictive in the complete group (n = 171) for arrhythmic events during follow-up (13 +/- 6 months, range 6 to 24) (hazard ratio 7.7, p < 0.02, Cox proportional-hazards survival analysis), but treatment (streptokinase vs conventional) did not significantly affect outcome when added to the model. It is concluded that thrombolysis prevents the development of late potentials. However, this study does not confirm the hypothesis that prevention of late potentials leads to a decrease in arrhythmic events.


Assuntos
Arritmias Cardíacas/prevenção & controle , Eletrocardiografia/efeitos dos fármacos , Infarto do Miocárdio/tratamento farmacológico , Estreptoquinase/uso terapêutico , Terapia Trombolítica , Adulto , Idoso , Idoso de 80 Anos ou mais , Arritmias Cardíacas/etiologia , Morte Súbita Cardíaca/etiologia , Eletrocardiografia/métodos , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/patologia , Infarto do Miocárdio/fisiopatologia , Recidiva , Taxa de Sobrevida , Taquicardia Ventricular/etiologia , Fibrilação Ventricular/etiologia
8.
Am J Cardiol ; 70(11): 990-6, 1992 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-1384304

RESUMO

The electropharmacologic effects and pharmacokinetics of almokalant, a new class III antiarrhythmic, were investigated in a randomized, placebo-controlled, double-blind study, and efficacy was evaluated. Ten post-myocardial infarction patients with complex ventricular arrhythmias were included and received, in randomized order on consecutive days, 4.5 mg (12.8 mumol) of almokalant or placebo intravenously over 10 minutes. One patient received infusion at a higher rate and developed self-terminating torsades de pointes. In the remaining 9 patients the corrected QT interval increased significantly: At the end of placebo infusion the corrected QT was 445 +/- 18 ms and after almokalant 548 +/- 53 ms (p = 0.0015). The signal-averaged electrocardiographic parameters did not change. The number of ventricular premature complexes decreased significantly during the first 15 minutes after almokalant infusion (p = 0.04). No additional proarrhythmic or other significant adverse events were noted. The almokalant plasma concentration showed a biphasic decrease with an elimination half-life of 2.4 +/- 0.1 hours. Almokalant was rapidly cleared from the body with a clearance of 11 +/- 1 ml/min/kg. When given with certain precautions almokalant appears safe and well-tolerated and may be antiarrhythmic by prolonging refractoriness.


Assuntos
Antiarrítmicos/farmacologia , Antiarrítmicos/farmacocinética , Complexos Cardíacos Prematuros/fisiopatologia , Sistema de Condução Cardíaco/efeitos dos fármacos , Infarto do Miocárdio/fisiopatologia , Propanolaminas/farmacologia , Propanolaminas/farmacocinética , Adulto , Idoso , Método Duplo-Cego , Eletrocardiografia/métodos , Eletrocardiografia Ambulatorial , Feminino , Humanos , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Processamento de Sinais Assistido por Computador
9.
Am J Cardiol ; 68(11): 1194-202, 1991 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-1683146

RESUMO

Programmed electrical stimulation was performed in 12 patients with moderate to severe congestive heart failure and ventricular tachycardia (VT) to study possible arrhythmogenic properties of ibopamine, a new orally active dopamine agonist. Ibopamine induced no significant changes in spontaneous cycle length, PR, QRS, QTc, AH or HV intervals, and also right ventricular effective refractory periods were unaffected (for paced cycle lengths of 600 and 430 ms, respectively, using 1 extrastimulus: 287 +/- 16 ms at baseline vs 283 +/- 27 ms after ibopamine and 270 +/- 23 ms during the control study vs 262 +/- 19 ms after ibopamine). In 6 of the 8 patients with coronary artery disease but in none of the 4 patients with dilated cardiomyopathy, sustained VT was induced before and after ibopamine. Proarrhythmia was present in 1 patient, who became inducible after ibopamine. However, 1 patient had sustained VT only at baseline but not after ibopamine. The number of extrastimuli required for VT induction was equal (2.7 +/- 0.2 vs 2.7 +/- 0.2). Holter monitoring showed no changes in ventricular premature complexes, ventricular couplets and runs of VT after 1 week of ibopamine therapy. The signal-averaged electrocardiogram was abnormal in 11 and showed late potentials in 5 patients, but no changes occurred after ibopamine. During hemodynamic evaluation, increases in cardiac (32%) and stroke volume (34%) indexes were seen after administration of 100 mg of ibopamine, accompanied by a decrease in vascular resistance and filling pressures. Plasma norepinephrine decreased significantly after ibopamine (p = 0.02) but plasma epinephrine was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)


Assuntos
Catecolaminas/sangue , Desoxiepinefrina/análogos & derivados , Dopaminérgicos/farmacologia , Insuficiência Cardíaca/fisiopatologia , Hemodinâmica/efeitos dos fármacos , Taquicardia/fisiopatologia , Adulto , Idoso , Pressão Sanguínea/efeitos dos fármacos , Estimulação Cardíaca Artificial , Desoxiepinefrina/uso terapêutico , Eletrocardiografia/efeitos dos fármacos , Eletrocardiografia Ambulatorial , Feminino , Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/tratamento farmacológico , Humanos , Masculino , Pessoa de Meia-Idade , Volume Sistólico/efeitos dos fármacos , Taquicardia/complicações , Resistência Vascular/efeitos dos fármacos
10.
Coron Artery Dis ; 7(3): 225-30, 1996 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-8827409

RESUMO

METHODS: Sixty-nine patients with sustained ventricular tachyarrhythmias were followed up to evaluate the predictive value of functional capacity (i.e., New York Heart Association class and peak oxygen consumption) and resting left ventricular function (i.e. radionuclide left ventricular ejection fraction, angiographic left ventricular wall motion score and echocardiographic dimensions) with respect to arrhythmia recurrence. RESULTS: During a mean follow-up of 19 months 18 patients (26%) had an arrhythmia recurrence. Parameters of functional capacity and echocardiographic dimensions were not related to arrhythmia recurrence. Left ventricular ejection fraction and wall motion score were worse in patients with a recurrence compared with the arrhythmia-free patients: 30 +/- 16% versus 40 +/- 19% (mean +/- SD, P = 0.035) and 25 +/- 7 versus 20 +/- 7 (P = 0.01), respectively. Multivariately the most powerful parameter was left ventricular wall motion score (odds ratio 1.12, 95% Cl 1.02-1.23). CONCLUSIONS: Arrhythmia recurrence in ventricular tachyarrhythmia patients relates to resting left ventricular function and not to functional capacity. Since angiographic left ventricular wall motion score is prognostically more important than ejection fraction this parameter should be considered for risk stratification in these patients.


Assuntos
Angiografia Coronária/métodos , Taquicardia Ventricular/diagnóstico por imagem , Disfunção Ventricular Esquerda/fisiopatologia , Fibrilação Ventricular/diagnóstico por imagem , Idoso , Angioplastia Coronária com Balão , Antiarrítmicos/uso terapêutico , Teste de Esforço , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Recidiva , Taquicardia Ventricular/fisiopatologia , Taquicardia Ventricular/terapia , Disfunção Ventricular Esquerda/diagnóstico por imagem , Disfunção Ventricular Esquerda/terapia , Fibrilação Ventricular/fisiopatologia , Fibrilação Ventricular/terapia
11.
Int J Cardiol ; 38(3): 293-8, 1993 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-8463010

RESUMO

AV nodal tachycardia may present at any age, but onset in late adulthood is considered uncommon. To evaluate whether onset of AV nodal tachycardias at older age is related to organic heart disease (possibly setting the stage for re-entry due to degenerative structural changes) 32 consecutive patients with symptomatic AV nodal tachycardia were studied. The age at onset of attacks showed a bimodal pattern, with 2 peaks: one between 15 and 35 years (22 patients) and one around 55 years (10 patients). Significantly more older patients had an underlying heart disease (60% versus 14%, P < 0.01), with coronary artery disease in 4 and hypertensive heart disease in 3. Frequent supraventricular ectopic activity was seen during baseline 24-h ambulatory monitoring in all the older patients, versus in only half of the younger patients (P = 0.005). These results indicate that late onset AV nodal tachycardia (i.e. > age 45 years) is not infrequent (33%). The frequent supraventricular arrhythmias on one hand and age-related structural AV nodal changes, potentially enhanced by underlying heart disease on the other, both may contribute to the development of late onset re-entrant AV nodal tachycardia.


Assuntos
Cardiopatias/complicações , Taquicardia por Reentrada no Nó Atrioventricular/etiologia , Adulto , Fatores Etários , Estimulação Cardíaca Artificial , Eletrocardiografia , Eletrocardiografia Ambulatorial , Feminino , Sistema de Condução Cardíaco/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Taquicardia por Reentrada no Nó Atrioventricular/diagnóstico , Taquicardia por Reentrada no Nó Atrioventricular/epidemiologia
12.
Int J Cardiol ; 46(2): 121-8, 1994 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-7814160

RESUMO

In a series of 171 consecutive survivors of acute myocardial infarction, the predictive value of late potentials and QTc prolongation was prospectively assessed. QT intervals were measured in lead V2, corrected QT (QTc) was calculated using Bazett's equation (cut-off value 440 ms). Late potentials were considered to be present when all of the three signal-averaged electrocardiographic variables were abnormal (i.e. QRS > 114 ms, D40 > 38 ms, and V40 < 20 microV). Complete follow-up was obtained (mean 13 +/- 6 months, range 6-24 months). Six percent of the patients had an arrhythmic event (i.e. sustained ventricular tachycardia or sudden death). The relative risk of late potentials for arrhythmic events was 7.7 (P < 0.02). The relative risk of QTc > 440 ms was 1.1 (NS). In a multivariate analysis, the addition of QTc prolongation did not significantly improve the prognostic value of late potentials alone. It is concluded that late potentials are predictive of arrhythmic events after myocardial infarction, but the presence of concomitant QTc prolongation does not worsen the prognosis.


Assuntos
Arritmias Cardíacas/etiologia , Infarto do Miocárdio/complicações , Potenciais de Ação , Idoso , Arritmias Cardíacas/diagnóstico , Arritmias Cardíacas/tratamento farmacológico , Arritmias Cardíacas/epidemiologia , Arritmias Cardíacas/fisiopatologia , Intervalos de Confiança , Eletrocardiografia , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio/mortalidade , Infarto do Miocárdio/fisiopatologia , Valor Preditivo dos Testes , Estudos Prospectivos , Tempo de Reação , Fatores de Risco , Processamento de Sinais Assistido por Computador , Taxa de Sobrevida
13.
Int J Cardiol ; 93(2-3): 231-7, 2004 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-14975552

RESUMO

UNLABELLED: Twenty-five patients (16 males, mean age 46 years) underwent radiofrequency ablation because of either paroxysmal (13 patients) or persistent atrial fibrillation (12 patients). Ablation aimed at earliest activation of spontaneous and catheter-induced repetitive ectopy in left and right atria and appendages, and pulmonary veins. Catheter-induced repetitive ectopy was defined as acute onset of a burst of rapid atrial premature beats on touching the wall, sustained irritability while at the spot and acute termination of rapid activity upon release of the catheter. Post-ablation patients received antiarrhythmic drugs to prevent tachycardias, thereby allowing reversal of atrial remodeling. RESULTS: Lone atrial fibrillation was present in 19 patients, 4 patients had hypertension and 2 patients coronary artery disease with preserved left ventricular function. The median duration of the history of atrial fibrillation was 4 years (range 1-14 years) and the median number of antiarrhythmic drug failures 5 (range 1-6). Ablation was successful, i.e. no recurrences of atrial fibrillation with or without antiarrhythmic drugs in eight patients (32%) during a median follow-up of 28 months (range 18-52). The median number of foci was 3 (range 2-6) and 2 (range 1-7) in the successfully and unsuccessfully treated patients, respectively. Minor complications occurred in three patients. CONCLUSIONS: Radiofrequency ablation of atrial fibrillation aiming at spontaneous and catheter-induced repetitive ectopy is a safe procedure. However, it is only successful in one third of the patients. Further investigations are warranted to identify the ideal patient, as well as to develop better ablation strategies.


Assuntos
Fibrilação Atrial/cirurgia , Ablação por Cateter , Antiarrítmicos/uso terapêutico , Eletrocardiografia , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Seleção de Pacientes , Fatores de Tempo
14.
Clin Cardiol ; 16(3): 270-2, 1993 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-8444004

RESUMO

Digitalis intoxication is one of the most common adverse drug reactions. Although some arrhythmias are seen more frequently than others, virtually any rhythm disturbance, including ventricular tachycardia, may occur. However, to our knowledge, exercise-induced ventricular tachycardia as a complication of digitalis therapy has never been described before. This case presents a patient with a digitalis-induced ventricular tachycardia occurring exclusively during exercise.


Assuntos
Digoxina/efeitos adversos , Taquicardia Ventricular/induzido quimicamente , Eletrocardiografia , Teste de Esforço/efeitos dos fármacos , Feminino , Humanos , Pessoa de Meia-Idade , Taquicardia Ventricular/diagnóstico
15.
Clin Cardiol ; 15(9): 689-92, 1992 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-1395204

RESUMO

In a woman with an old infarction and sustained ventricular tachycardia, tachycardias were only inducible after short-long RR sequences. After isoprenaline, tachycardias became incessant and all were preceded by short-long RR sequences. This strongly suggests that triggered activity plays a role in initiation of ventricular tachycardias in postinfarction patients.


Assuntos
Infarto do Miocárdio/complicações , Taquicardia Ventricular/etiologia , Idoso , Estimulação Cardíaca Artificial , Estimulação Elétrica , Eletrocardiografia , Teste de Esforço , Feminino , Humanos , Isoproterenol/farmacologia , Taquicardia Ventricular/fisiopatologia
16.
Ned Tijdschr Geneeskd ; 148(48): 2396-402, 2004 Nov 27.
Artigo em Holandês | MEDLINE | ID: mdl-15615276

RESUMO

Two men aged 47 and 56 and one woman aged 21 presented at our cardiology department with presyncope, heart failure and exercise induced palpitations, respectively. Using the criteria of McKenna et al., a diagnosis of arrhythmogenic right-ventricular cardiomyopathy (ARVC) was made. Following implantation of a defibrillator, one of the men experienced seven appropriate interventions within six months and also developed psychological problems. The other man was problem-free and the woman recovered reasonably well, having only one appropriate intervention from the defibrillator one year after implantation. Indications of ARVC were also found in her mother but not in any other family members. Because ARVC manifests itself in various different ways it is difficult to diagnose. It is important to consider ARVC in patients with exercise-induced palpitations, presyncope, and unexplained cardiomyopathies or arrhythmias, especially if there is a family history of unexpected deaths. ARVC is a potentially life-threatening disease, that may require implantation of a cardioverter defibrillator. Furthermore, since genetics play an important role and ARVC can be asymptomatic, evaluation of close relatives for preclinical symptoms is important.


Assuntos
Displasia Arritmogênica Ventricular Direita/diagnóstico , Displasia Arritmogênica Ventricular Direita/terapia , Morte Súbita Cardíaca/prevenção & controle , Desfibriladores Implantáveis , Adulto , Displasia Arritmogênica Ventricular Direita/complicações , Displasia Arritmogênica Ventricular Direita/genética , Diagnóstico Diferencial , Eletrocardiografia , Feminino , Predisposição Genética para Doença , Humanos , Masculino , Pessoa de Meia-Idade
17.
Neth Heart J ; 16(6): 189-90, 2008 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-18665202
20.
Neth Heart J ; 18(12): 583-91, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21301620

RESUMO

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is an inherited cardiac disease with reduced penetrance and a highly variable expression. Mutations in the gene encoding the plakophilin-2 gene (PKP2) are detected in about 50% of ARVC/D patients. The p.Arg79X mutation in PKP2 has been identified in Europe and North America and has been functionally characterised. We evaluated the prevalence of the p.Arg79X mutation in PKP2 in the Dutch population. METHODS: Twelve index patients and 41 family members were evaluated in three university hospitals in the Netherlands. The diagnosis of ARVC/D was established according to the recently revised Task Force Criteria. Segregation of the p.Arg79X mutation was studied and haplotypes were reconstructed to determine whether the p.Arg79X mutation was a recurrent or a founder mutation. RESULTS: The p.Arg79X mutation in PKP2 was identified in 12 index patients. Haplotype analysis revealed a shared haplotype among Dutch p.Arg79X mutation carriers, indicating a common founder. Six index patients (50%) had a first- or second-degree relative who had died of sudden cardiac death below 40 years of age. At age 60, only 60% of the mutation carriers had experienced any symptoms. There was no significant difference in symptom-free survival and event-free survival between men and women. CONCLUSION: We have identified the largest series of patients with the same desmosome gene mutation in ARVC/D reported to date. This p.Arg79X mutation in PKP2 is a founder mutation in the Dutch population. The phenotypes of PKP2 p.Arg79X mutation carriers illustrate the clinical variability and reduced penetrance often seen in ARVC/D. (Neth Heart J 2010;18:583-91.).

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