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Two types of progressive familial heart block controlled by a single gene have been described; 4 cases show that type I is progressive and that the pathogenesis is still unknown.
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Marfan's syndrome is classified as a heritable disorder of connective tissue in which the supporting structure is involved in clinical and pathologic alterations. In its classic form the syndrome is associated with abnormalities of the eye, aorta, and the skeleton. Conduction disturbances and ventricular arrhythmias have rarely been described in this syndrome. In this brief case report a patient with symptomatic heart block, prolonged atrial-His interval and ventricular arrhythmia in whom a permanent ventricular pacemaker has been implanted, is described.
We report a case of transient complete heart block following occlusion of the first septal perforator branch after stent deployment in the left anterior descending coronary artery. The patient was treated with temporary transvenous pacing and reverted spontaneously to normal atrioventricular conduction after 3 days.
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OBJECTIVE: Overexpression of calcineurin causes cardiac hypertrophy and arrhythmic deaths. During disease development, sinus bradycardia followed by high degree atrioventricular (AV) block finally culminating in ventricular asystole has been observed over time in calcineurin hearts. AV block is associated with the development of pleomorphic ventricular tachycardia in mice and downregulation of potassium currents in ventricular myocytes. We tested the hypothesis that the abnormalities of AV block and propensity to ventricular tachycardia relate to overexpression of calcineurin independent of the development of hypertrophy. METHODS: Cardiac electrophysiologic properties were compared in isolated perfused hearts with ventricular hypertrophy due to overexpression of calcineurin or NF-AT3 and in their corresponding wild types at 15 or 30 days of age. RESULTS: Compared to wild-type hearts, significant prolongation of sinus node recovery times was noted in both NF-AT3 and calcineurin hearts. Compared to wild-type hearts, Wenckebach cycle length (WCL) and the left ventricular effective refractory period (LVERP) were significantly prolonged in the calcineurin hearts (p<0.05) but not NF-AT3 hearts. In calcineurin mice, left ventricular effective refractory period impinged on Wenckebach cycle length resulting in a significant correlation between left ventricular effective refractory period and Wenckebach cycle length (r(2)=0.56). No such correlation was observed for wild type or NF-AT3 hearts. At 30 days of development, ventricular tachycardia developed in 70% of calcineurin hearts compared to 0% wild-type hearts (p=0.003), whereas ventricular tachycardia was observed in 33% of NF-AT3 hearts and 10% of corresponding wild-type hearts (p=NS). CONCLUSIONS: The prolonged ventricular refractoriness, seen only in calcineurin hearts, impinges on Wenckebach cycle length resulting in heart block and is associated with propensity to ventricular tachycardia.
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BACKGROUND: The aim of this study was to evaluate the clinical features of patients with congenital complete heart block (CCHB) who developed dilated cardiomyopathy (DCM) after pacemaker implantation (PMI) and to determine factors predicting DCM development. METHOD: A total of 15 patients were reviewed retrospectively. They were classified into two groups, one consisted of four patients who were diagnosed as having CCHB in utero or at birth and who developed DCM after PMI (DCM group) and the other consisted of 11 patients who did not (non-DCM group). RESULTS: Maternal autoantibodies were found in two of the DCM group and in five of the non-DCM group. Perfusion defects in myocardial imaging were detected in all DCM patients and in five non-DCM patients. DCM developed 2 to 43 months after PMI and three DCM patients died of heart failure 7 to 48 months after PMI. In pathological studies, endocardial or interstitial fibrosis was present in all DCM patients and in one of two in the non-DCM group. No significant differences between the two groups were found in age at PMI, atrial or ventricular rate, end-diastolic dimension and ejection fraction of the left ventricle before PMI, and width of QRS after PMI. CONCLUSION: Although it was suspected that the patients with CCHB had myocardial involvement before PMI, there was no significant factor predicting the risk of DCM after PMI. In addition to cardiac rhythm abnormalities, careful attention should be paid to cardiac function in CCHB patients after PMI.
Severe hypothyroidism in children is known to produce cardiac abnormalities such as asymmetric thickening or hypertrophy of the interventricular septum, smaller internal dimensions of the left ventricle, a smaller left ventricular outflow tract, and less systolic septal excursion. In this report, we present a 1.5-year-old boy who was admitted to our hospital because of growth retardation. According to the clinical and laboratory findings, congenital hypothyroidism, dilated cardiomyopathy (DCMP), atrioventricular complete heart block and secundum type atrial septal defect were diagnosed.
A 57-year-old female presented with complete heart block and then developed refractory hypotension despite temporary pacing. Moderate left ventricular dysfunction with focal wall motion abnormalities, as well as severe hypoxemia, were demonstrated. However, neither significant coronary disease nor evidence for pulmonary embolus or other lung disease could be determined. Hemodynamic stabilization was achieved with the use of an intra-aortic balloon pump and multiple high-dose pressor agents. A retrospective diagnosis of toxic verapamil-SR and atenolol ingestion was confirmed, and the patient gradually recovered. The relevant literature is reviewed and various treatment approaches are discussed.
The radiographic findings in 13 patients with congenital complete heart block without associated anomalies are presented to illustrate characteristic features. Findings related to the increased stroke volume in these patients include: (a) simulated shunt vasculature; (b) pulmonary venous pypertension with redistribution of blood flow to the upper lungs, and, in one patient, peribronchial edema; (c) cardiomegaly with right ventricular, pulmonary artery, left atrial, left ventricular, and aortic enlargement; and (d) variation in cardiac size on serial examinations. Less commonly seen were findings related to atrioventricular dissociation with transitory marked pulmonary venous hypertension present in one patient when left atrial contraction occurred during ventricular systole when the mitral valve was closed.
Two White male patients with temporary complete heart block (CHB) secondary to hyperkalaemia are presented. One, a 40-year-old man, developed CHB with ensuing shock within the first 24 hours of repeat aortic valve replacement for a paraprosthetic leak caused by previous endocarditis. This patient experienced iatrogenic hyperkalaemia. The second was an 81-year-old man who had chronic renal failure and presented with Stokes-Adams attacks. This patient was initially thought to have degenerative CHB and nearly underwent inadvertent permanent pacemaker insertion. Both patients were initially treated with emergency temporary cardiac pacing with subsequent successful management. Temporary CHB secondary to hyperkalaemia, from whatever cause, has very rarely been documented in the literature. A review of this potentially lethal complication is undertaken and the significance of unifascicular and bifascicular conduction block as a consequence of hyperkalaemia is discussed.
The aim of this study was to examine 24h patterning in the symptoms indicative of third-degree atrio-ventricular (AV) heart block. We found a total of 227 cases (126 men and 101 women) of third-degree AV block that had been diagnosed by the Emergency Medical Department of the St. Anna Hospital in Ferrara, Italy between 1990 and 2001. Determination of the hour of onset of symptomatic third-degree AV block, however, was possible and listed in the records of only 161 or 70.9% of the cases (92 men and 69 women). The onset time of every event was categorized into one of four 6h spans of the 24h: night (00:00-05:59h), morning (06:00-11:59h), afternoon (12:00-17:59h), and evening (18:00-23:59h). The onset of the symptoms of third-degree AV block in the sample of 161 cases was significantly greater in the morning between 06:00 and 11:59h than any other 6h span of the day and night (chi2-test; p < 0.001). The same phenomenon was substantiated in the subgroup of the 92 males (chi2; p < 0.0001), although it could not be detected for the smaller subgroup of 69 women. The 24h pattern, with morning preference, in the onset of symptomatic third-degree AV block is similar to the one in sudden cardiac death and cardiogenic cardiac arrest. The etiology of the 24h pattern in symptomatic AV block is unknown; it may be an expression of intrinsic biological rhythmicity within the heart tissue or its control system, and/or the timing of environmental triggers resulting in coronary ischemia.
This case report presents a young adult with asymmetric septal hypertrophy (ASH) and syncope. Infranodal complete heart block was demonstrated as his cause for syncope. Therapy consisted of implantation of a A-V sequential pacemaker. Cardiac output determinations and systolic time intervals demonstrated the beneficial effects of properly timed atrial contractions.
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A significant age dependence of the risk of complete heart block complicating radiofrequency ablation of the AV nodal slow pathway was noticed, with no patients <45 years of age experiencing this complication.
Maternal IgG autoantibodies against Ro52 (part of the anti-SSA specificity) are correlated with congenital heart block (CHB). Most cases revert spontaneously and can be monitored by Doppler echocardiography, but fetuses that progress into second-degree block require treatment with, e.g., corticosteroids. A third-degree block is irreversible and necessitates lifelong pacemaking. It may prove beneficial to screen all expectant mothers for anti-Ro52 autoantibodies. Decisions about this will require further studies of the diagnostic performance of the Ro52 autoantibody test.
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