Naoki Matsuda

Idiopathic Ventricular Fibrillation Induced With Vagal Activity in Patients Without Obvious Heart Disease

BACKGROUNDnRecently, idiopathic ventricular fibrillation (VF) has gained much attention. Although several subgroups have been described, its pathogenesis, mechanism, treatment, and prognosis remain unknown.nnnMETHODS AND RESULTSnWe studied six cases of idiopathic VF with transient late r waves and ST elevation (late r/ST elevation) in leads V1 through V3. Late r/ST elevation was augmented before and after VF episodes. Signal-averaged ECGs showed late potentials even when no late r/ST elevation occurred. During late r, a conduction delay was observed by use of body-surface maps at the anterior wall and outflow tract of the right ventricle without inhomogeneity of the repolarization phase. There was a decrease or total disappearance of late r/ST elevation with isoproterenol, atropine, and exercise stress testing and induction or exacerbation with propranolol, edrophonium, and hyperventilation. VF was induced by programmed electrical stimulation in all cases but two, in which it was induced only after edrophonium injection. In two cases, VF was exacerbated by propranolol, and in all cases, it was uninducible with isoproterenol. Heart rate spectral analysis just before VF episodes showed a sudden rise in vagal activity in two cases. As the VF mechanism, a conduction delay exists at the anterior wall and outflow tract of the right ventricle that is possibly exacerbated by an abrupt rise in vagal activity, inducing random reentry that results in VF. Class I antiarrhythmic agents and beta-blockers were ineffective for this VF. All subjects required implantable cardioverter-defibrillators.nnnCONCLUSIONSnWe propose this VF associated with late r/ST elevation in the precordial leads and influenced by vagal activity as a new possible mechanism of idiopathic VF.

Enhancement of the L-Type Ca2+ Current by Mechanical Stimulation in Single Rabbit Cardiac Myocytes

Anion conductance is known to be activated by mechanical stimulation, such as osmotic cell swelling or cell inflation via the patch pipette, of canine or rabbit cardiac myocytes. The effects of mechanical stimulation on time-dependent currents, however, remain unsettled. Using the whole-cell voltage-clamp method, we have found that mechanical stimuli enhance the L-type Ca2+ current (ICa,L) in rabbit cardiac myocytes. At every membrane potential, ICa,L was reversibly increased by osmotic cell swelling and by cell inflation caused by applying a positive pressure of 10 to 15 cm H2O via the patch pipette. ICa,L was increased during cell inflation by 37 +/- 21% (mean +/- SD, n = 17) in atrial cells and by 37 +/ -8% (n = 7) in sinoatrial node cells in solution containing 2 mmol/L Ca2+. The current-voltage relationship, the inactivation time constant, the steady state inactivation curve, and the conductance properties of ICa,L were all virtually unaffected by mechanical stimulation except for the open probability, which appears to increase. The increase in ICa,L was not dependent on protein kinase A, since an inhibitor peptide of cAMP-dependent protein kinase failed to prevent the increase in ICa,L during mechanical stimuli (n=5). The increase in ICa,L caused by cell inflation was unaffected by the chelation of intracellular Ca2+ by the addition of 10 mmol/L EGTA or 10 mmol/L BAPTA to the pipette solution, suggesting that the effect was not mediated by changes in intracellular Ca2+. Thus, mechanical stimulation due to cell swelling or inflation may itself directly increase ICa,L in rabbit cardiac myocytes.

Contact Sensitivity to Polychloroparaxylene‐Coated Cardiac Pacemaker

Poly‐chloroparaxylene (parylene) is widely used as a material for cardiac pacemaker coating. Contact sensitivity to parylene was proven by patch test. Wrapping the pacemaker in a polytetrafluoroethylene sheet prior to implantation prevented further skin reactions.

Postoperative therapy using human atrial natriurectic peptide in cases of valve replacement

The effect of hANP (atrial natriuretic peptide) was investigated clinically in 40 patients who underwent isolated valve replacement. Patients were divided into four groups: aortic regurgitation (AR), aortic stenosis (AS), mitral regurgitation (MR) and mitral stenosis (MS). Each group was divided into two subgroups: one was administered hANP after the operation until leaving ICU, and the other was not administered hANP. We measured the levels of hANP and c-GMP and blood pressure, pulmonary artery pressure, central venous pressure and levels of Na, K of urine and blood prcoperatively, immediately postoperatively and 1, 2, 4, 6 hours after operation. First, to examine the relationship between preoperative level of hANP and cardiac function, the relationship between preoperative level of hANP and history of cardiac failure and pulmonary artery wedge pressure (PAWP) were evaluated. Also, we evaluated the relationship between preoperative level of hANP and each dimension on echocardiography. There was a weak statistical relationship between hANP and PAWP (row = 0.39 (p = 0.04) Pearson correlation method) and there was no statistical relationship between hANP and duration of cardiac failure (row = 0.00445 (p = 0.98) Pearson correlation method). Preoperatively Left atrial diameter (LAD) showed a statistical relationship with level of hANP in every group using Spearman correlation method. Other dimensions such as left ventricular diastolic diameter (LVDd) and left ventricular systolic diameter (LVDs) and also fractional shortening (FS) did not show a strong correlation with preoperative level of hANP. Especially, in AS group there was a strong relationship between every dimension and preoperative level of hANP. Only in MS group LAD and the level of hANP were negatively related. This finding suggests that atrial dilatation results in reduction of secretion of hANP in cases of MS on long term follow up. Finally, hNAP therapy was shown to have a continuous diuretic effect, with stable hemodynamics.

ICD Therapy: Can It Prevent Sudden Death in CHF Patients?

Implantable cardioverter defibrillator (ICD) therapy has greatly decreased the risk of sudden death in patients with reduced heart function. However, the ICD may be limited in improving the prognosis in these patients. More patients who received consecutive discharges died than did those patients who received only single discharges or no discharges at all. In our study, six of seven patients with severely reduced heart function who had consecutive discharges died. Treatment with only ICD therapy may be limited in improving the prognosis in these patients, and therefore we should consider using amiodarone or a β-blocker combined with ICD therapy. In our study, there was no difference in the number of patients who received ICD discharges between those treated or not treated with amiodarone plus β-blockers. However, there were no patients who received consecutive discharges or who died in the group of patients treated with amiodarone plus β-blockers. Our findings suggested that although concomitant therapy with amiodarone plus β-blockers was effective in increasing the electrical stability necessary to terminate VT/VF by a single discharge from an ICD, and this effect contributed to improving the prognosis.

Volume-regulated cardiac ion channels

Volume regulation is a feature common to many excitable cells including epithelial and peripheral blood cells [1,2]. The volume regulatory decrease (RVD) following osmotic cell swelling mainly results from the loss of KCl and water within the cell [3]. Thus, both K+ and Cl− conductive pathways have been suggested to be responsible for the volume regulation in various cell species. In cardiac cells, swelling-activated Cl− current (volume-regulated Cl− current) has been found in canine atrial and ventricular cells as well as rabbit sinoatrial node and atrial cells by superfusing the cells with hypotonic external solution or by inflating the cell through the patch pipette [4–6]. Since cell swelling occurs during myocardial ischemia or reperfusion [7], swelling-activated Cl− current may contribute to the volume regulatory process in patho-physiological conditions. In this chapter, we describe the conductive pathway, kinetic properties and mechanisms of activation of volume-regulated Cl− current and its possible contribution to the volume regulatory process in cardiac myocytes.

Stretch-Activated Current in Rabbit Cardiac Myocytes

The stretch-activated (SA) ion channels have been widely observed in various excitable cell membranes [1–3], and SA channels are now considered to play an important role in mechano-transduction. In cardiac myocytes, existence of SA channels has not yet been identified both in the whole-cell voltage clamp and single channel current. In the present study, we found a CI¯ conductance in response to membrane stretch in isolated sinoatrial node and atrial cells. The Cl -conductance activated by stretch was determined from reversal potential measurements, and from the blocking effect of various CI¯ channel blockers. The only CI¯ currents described in detail so far are the catecholamine-induced CI¯ current [4–6] and the Ca2+-activated CI¯ current [7] in cardiac cells. The stretch-activated CI¯ current is different from the CI¯ currents which were activated by catecholamine or intracellular Ca2+. Since mechanical stimulations are continuously present in the intact cardiac tissue, stretch-activated CI¯ current may contribute to the action potential of cardiac myocytes under physiological conditions.