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Paul Milliez

Publications and source records attributed to Paul Milliez.

At least 19 recordsLinked to original sources
PubMed2006

Atrioventricular nodal reentrant tachycardia associated with idiopathic ventricular tachycardia: clinical and electrophysiologic characteristics.

BACKGROUND: Case reports have described the coexistence of ventricular tachycardia (VT) and supraventricular tachycardia in the same patient. This study examines the frequency of dual atrioventricular nodal (AVN) physiology, AVN echo beats, and atrioventricular nodal reentrant tachycardia (AVNRT) in patients with VT. METHODS: Programmed atrial and ventricular stimulation was performed in 132 consecutive patients referred for electrophysiologic study of symptomatic VT. Of the 132, 99 patients had structural heart disease, and 33 patients had idiopathic ventricular tachycardia (IVT). RESULTS: Among the 33 patients with IVT, 23 had dual AVN physiology. Compared with patients with structural heart disease undergoing VT ablation, dual AVN pathways (70% vs 27%, P < .0001), dual AVN pathways with echo beats (24% vs 8%, P = 0.03), and AVNRT (21% vs 1%, P = .0002) were more common in patients with IVT. CONCLUSION: Dual AVN physiology and AVNRT appear to be associated with IVT. This finding suggests that patients with IVT should undergo a complete electrophysiologic evaluation, and the diagnosis of coexistent AVNRT should be considered in this population.

Adolescent↗
PubMed2006

Chronic hemodynamic overload of the atria is an important factor for gap junction remodeling in human and rat hearts.

OBJECTIVES: The expression and distribution of connexins is abnormal in a number of cardiac diseases, including atrial fibrillation, and is believed to favor conduction slowing and arrhythmia. Here, we studied the role of atrial structural remodeling in the disorganization of gap junctions and whether redistributed connexins can form new functional junction channels. METHODS: Expression of connexin-43 (Cx43) was characterized by immunoblotting and immunohistochemistry in human right atrial specimens and in rat atria after myocardial infarction (MI). Gap junctions were studied by electron and 3-D microscopy, and myocyte-myocyte coupling was determined by Lucifer yellow dye transfer. RESULTS: In both chronically hemodynamically overloaded human atria in sinus rhythm and in dilated atria from MI-rats, Cx43 were dephosphorylated and redistributed from the intercalated disc to the lateral cell membranes as observed during atrial fibrillation. In MI-rats, the gap junctions at the intercalated disc were smaller (20% decrease) and contained very little Cx43 (0 or 1 gold particle vs. 42 to 98 in sham-operated rats). In the lateral membranes of myocytes, numerous connexon aggregates comprising non-phosphorylated Cx43 were observed. These connexon aggregates were in no case assembled into gap junction plaque-like structures. However, N-cadherin was well organized in the intercalated disc. There was very little myocyte-myocyte coupling in MI-rat atria and no myocyte-fibroblast coupling. Regression of the atrial remodeling was associated with the normalization of Cx43 localization. CONCLUSION: Structural alteration of the atrial myocardium is an important factor in the disorganization of connexins and gap junction. Moreover, redistributed Cx43 do not form junction channels.

Animals↗
PubMed2006

Quantitative assessment of ST segment elevation in Brugada patients.

BACKGROUND: ST segment elevation in the right precordial leads constitutes the electrocardiogram (ECG) hallmark of Brugada syndrome (BS). This pattern is variable and can be concealed, but the magnitude and the cause of ST segment fluctuations have been poorly investigated. OBJECTIVE: Our goal was to quantify ST changes and to assess rate and autonomic influences on ST level. METHODS: A 12-lead ECG was continuously recorded during 24 hours in 20 patients with BS (ages 49 +/- 12) and 10 healthy subjects (ages 32 +/- 7). Using two-dimensional binning we obtained average QRS-T complexes every 30 minutes (time bins) and at different RR intervals (rate bins) for each subject. ST level was measured at five different points located 90, 100, 110, 120, and 140 ms after Q onset (Qo). In BS patients, the highest ST elevation was measured 110 ms after Qo (Qo+110). RESULTS: ST level changes between time points were significantly greater in patients with BS compared with control subjects: on lead V2, the range of ST level at Qo+110 was 264 +/- 85 microV in BS and 91 +/- 22 microV in control subjects (P <.01). In BS, ST level decreased with heart rate acceleration: the difference in ST level at Qo+110 for RR = 900 and 600 ms was 55 +/- 53 microV (P <.01). HFnu was positively, although weakly, correlated with ST level (R(2) = 0.02, P <.01). CONCLUSIONS: ECG changes observed in patients with BS are related in part to heart rate influences on ST segment level. These spontaneous fluctuations over a 24-hour time period suggest that Holter recordings may improve the ECG diagnosis sensitivity in BS.

Adult↗
PubMed2005

Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction.

AIMS: Congestive heart failure (CHF) is associated with severe structural changes of atria, contributing to impaired atrial function and the risk of arrhythmia. This study investigated the effects of CHF treatments on atrial remodelling. METHODS AND RESULTS: Three months after myocardial infarction (MI), rats were treated for 1 month with spironolactone, lisinopril, or atenolol alone or in combination. Echocardiography-Doppler tissue imaging, haemodynamic measurements, and 24-h Holter monitoring were used to characterize the cardiomyopathy. Atrial fibrosis was quantified with Picrosirius Red staining. Left atrial diameter was increased (5.8+/-0.6 mm in MI vs. 3.6+/-0.3 mm in sham; P<0.0001), as was atrial fibrosis (26.7+/-3.8% in MI vs. 10.5+/-2.2% in sham; P<0.0001), which correlated with left ventricular (LV) dysfunction after 3 months of MI. P-wave duration was also increased and premature atrial beats were frequent on the 24-h electrocardiogram. Similar improvements in LV dysfunction were observed after 1 month of spironolactone, ACE-inhibitor, or beta-blocker therapy alone or in combination. Atrial hyperexcitability was reduced by all the treatments, but only spironolactone attenuated atrial fibrosis and reduced P-wave duration. CONCLUSION: Atrial fibrosis caused by chronic CHF is reduced by spironolactone.

Animals↗
PubMed2005

Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism.

OBJECTIVES: The aim of this report was to show that the rate of cardiovascular events is increased in patients with either subtype of primary aldosteronism (PA). BACKGROUND: Primary aldosteronism involves hypertension (HTN), hypokalemia, and low plasma renin. The two major PA subtypes are unilateral aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia. METHODS: During a three-year period, the diagnosis of PA was made in 124 of 5,500 patients referred for comprehensive evaluation and management. Adenomas were diagnosed in 65 patients and idiopathic hyperaldosteronism in 59 patients. During the same period, clinical characteristics and cardiovascular events of this group were compared with those of 465 patients with essential hypertension (EHT) randomly matched for age, gender, and systolic and diastolic blood pressure. RESULTS: A history of stroke was found in 12.9% of patients with PA and 3.4% of patients with EHT (odds ratio [OR] = 4.2; 95% confidence interval [CI] 2.0 to 8.6]). Non-fatal myocardial infarction was diagnosed in 4.0% of patients with PA and in 0.6% of patients with EHT (OR = 6.5; 95% CI 1.5 to 27.4). A history of atrial fibrillation was diagnosed in 7.3% of patients with PA and 0.6% of patients with EHT (OR = 12.1; 95% CI 3.2 to 45.2). The occurrence of cardiovascular complications was comparable in both subtypes of PA. CONCLUSIONS: Patients presenting with PA experienced more cardiovascular events than did EHT patients independent of blood pressure. The presence of PA should be detected, not only to determine the cause of HTN, but also to prevent such complications.

Adenoma↗
PubMed2005

Usefulness of ventricular repolarization dynamicity in predicting arrhythmic deaths in patients with ischemic cardiomyopathy (from the European Myocardial Infarct Amiodarone Trial).

The European Myocardial Infarct Amiodarone Trial (EMIAT) investigated the effects of amiodarone versus placebo in patients after myocardial infarction who had left ventricular ejection fraction </=40% and were </=75 years of age. The present substudy examined whether ventricular repolarization (VR) dynamicity could differentiate patients who died from cardiac death from their matched survivors in this EMIAT population. In addition, we assessed whether VR dynamicity could differentiate patients who died from arrhythmic cardiac death (ACD) and from non-ACD. VR dynamicity (determined from Holter's recordings at baseline) was compared before antiarrhythmic therapy in 118 patients who had cardiac death and 118 matched survivors according to age, gender, left ventricular ejection fraction, and subsequent administration or nonadministration of amiodarone. VR dynamicity was compared within the cardiac death group between the 59 patients who died from ACD and the 59 who died from non-ACD. VR dynamicity was expressed as the slope of the linear regression between QTo (measured automatically) and stable RR intervals. Patients who died were found to have a significant steeper rate dependence of QTo intervals during the 3 periods than their matched survivors. In multivariate analysis, the QTo/RR nocturnal interval appeared to be the best independent predictor of cardiac death. In addition, patients who died from ACD were found to have a significant steeper rate dependence of QTo intervals during the morning period than those who died from non-ACD. In the multivariate analysis, the QTo/RR morning interval remained the best independent predictor of ACD. Thus, in the EMIAT trial, evaluation of QT dynamicity is a strong predictor of cardiac death. In addition, QT dynamicity could predict the occurrence of ACD in cases of cardiac death.

Aged↗
PubMed2005

Spironolactone improves carotid artery fibrosis and distensibility in rat post-ischaemic heart failure.

Myocardial infarction causes neurohormonal activation involving aldosterone and angiotensin II (AngII). These hormones may increase arterial stiffness, an independent cardiovascular risk factor contributing to progression of congestive heart failure (CHF). This study aimed to determine the effect of aldosterone and AngII blockade on carotid artery distensibility and collagen density in adult Wistar rats with MI-induced CHF. Five groups were studied: Sham-operated, CHF, CHF + spironolactone, CHF + lisinopril, CHF + Spironolactone + Lisinopril. After echocardiography, in vitro isobaric carotid distensibility (echo-tracking technique) and collagen density were measured, and the incremental elastic modulus (Einc) calculated. In the CHF group, intra-ventricular pressure and cardiac weight were increased; carotid distensibility was reduced (CHF: 0.42 +/- 0.30 per mmHg(3) versus sham: 1.75 +/- 0.50 per mmHg(3); P < 0.001), and collagen content increased by 87% when compared to sham. All treatments reduced intra-ventricular pressure, carotid distensibility and fibrosis when compared to CHF but did not change cardiac weight. However, carotid distensibility and intra-ventricular pressure were not completely restored towards sham values and were significantly and inversely related. Spironolactone, which did not decrease significantly blood pressure, was the only drug reducing Einc independently of wall stress (WS). Thus, MI-induced CHF was associated with carotid artery remodeling. This vascular change, which may contribute to maintain cardiac hypertrophy and CHF, is largely prevented by AngII and aldosterone blockade. Only spironolactone reduced the stiffness of carotid wall material independently of blood pressure and WS.

Animals↗
PubMed2005

Cardiac and renal effects of levosimendan, arginine vasopressin, and norepinephrine in lipopolysaccharide-treated rabbits.

BACKGROUND: Because sepsis-induced myocardial dysfunction related to sepsis is at least partially related to a decrease in cardiac myofilament response to calcium, the use of the new myofilament-calcium sensitizer, levosimendan, has been proposed. In addition, arginine vasopressin is increasingly proposed as a vasopressor in septic patients, although data on its effects on cardiac function are still scarce. The aim of the current study was to assess, invasively and noninvasively, whether levosimendan, arginine vasopressin, and norepinephrine, either alone or combined, may modify sepsis-induced myocardial dysfunction and renal hemodynamics. METHODS: Thirty-six hours after lipopolysaccharide or saline administration, rabbits were studied either after slight sedation for echocardiography or after general anesthesia with sodium pentobarbital for the following measurements: aortic flow velocity and maximum acceleration of blood flow in the ascending aorta and renal macrocirculation and microcirculation. RESULTS: Levosimendan improved, within 30 min of administration, both maximum acceleration of blood flow by 20 +/- 12% (n = 8; P < 0.05) and left ventricular shortening fraction by a similar extent. Furthermore, low doses of arginine vasopressin markedly deteriorated cardiac function via an afterload-independent mechanism, even when animals were pretreated with levosimendan, whereas norepinephrine showed no detrimental effects on cardiac function. The study also showed that norepinephrine often improved renal medullary blood flow, whereas arginine vasopressin consistently decreased it. CONCLUSION: Levosimendan and norepinephrine both exert beneficial effects in endotoxemic animals and should be further explored in human sepsis trials.

Animals↗
PubMed2004

[Wolff-Parkinson-White syndrome].

WPW syndrome is a rare congenital heart disease due to an accessory pathway between the atrium and the ventricle. Its ECG pattern is characterized by a short PR interval, a delta wave, a wide QRS complex and an abnormal ventricular repolarisation. Patients are usually asymptomatic, or have frequent paroxysmal episodes of tachycardia. These tachycardias are supraventricular tachycardias related to either reentry between the AV node and the accessory pathway, or atrial tachyarythmias descending through this bypass tract, or both. In the latter clinical situation, sudden cardiac death may occur in case of short refractory period within the accessory pathway. An electrophysiologic study should be performed in order to characterize and localize this accessory pathway. If this pathway is capable of conducting rapidly anterogradely, we recommend an immediate radiofrequency ablation in both symptomatic and asymptomatic patients. In the contrary, medical or ablation therapy are indicated only in symptomatic patients.

Decision Trees↗
PubMed2004

Role of myocardial neuronal nitric oxide synthase-derived nitric oxide in beta-adrenergic hyporesponsiveness after myocardial infarction-induced heart failure in rat.

BACKGROUND: An emerging concept is that a neuronal isoform of nitric oxide synthase (NOS1) may regulate myocardial contractility. However, a role for NOS1-derived nitric oxide (NO) in heart failure (HF) has not been defined. METHODS AND RESULTS: Using a model of myocardial infarction-induced HF, we demonstrated that cardiac NOS1 expression and activity increased in HF rats (P<0.05 and P<0.001 versus shams, respectively). This was associated with translocation of NOS1 from the ryanodine receptor to the sarcolemma through interactions with caveolin-3 in HF hearts. With ex vivo and in vivo pressure-volume analysis, cardiac NOS1-derived NO was found to be negatively inotropic in shams but not HF hearts. Ventricular elastance (E(es)) was significantly reduced in HF rats (P<0.05), and tau, the time constant of left ventricular relaxation, was prolonged (both P<0.05). Acute NOS1 inhibition significantly increased E(es) by 33+/-3% and tau by 17+/-2% (P<0.05) in shams, although these effects were significantly attenuated in HF hearts. beta-Adrenergic stimulation induced a marked increase in systolic performance in sham hearts, with the responses being significantly blunted in HF hearts. E(es) increased by 163+/-42% (P<0.01) in sham hearts and 56+/-9% in HF hearts, and LV +dP/dt increased by 97+/-9% (P<0.01) in shams and 37+/-7% (P<0.05) in the HF group. Interestingly, preferential NOS1 inhibition enhanced the blunted responses of LV +dP/dt and E(es) to beta-adrenergic stimulation in HF rats but had no effect in shams. CONCLUSIONS: These results provide the first evidence that increased NOS1-derived NO production may play a role in the autocrine regulation of myocardial contractility in HF.

Adrenergic beta-Agonists↗
PubMed2004

Hydroquinidine therapy in Brugada syndrome.

OBJECTIVES: We sought to assess hydroquinidine (HQ) efficacy in selected patients with Brugada syndrome (BrS). BACKGROUND: Management of asymptomatic patients with BrS and inducible arrhythmias remains a key issue. Effectiveness of class Ia antiarrhythmic drugs, which inhibit the potassium transient outward current of the action potential, has been suggested in BrS. METHODS: From a cohort of 106 BrS patients, we studied 35 who received HQ (32 men; mean age 48 +/- 11 years). Patients had asymptomatic BrS and inducible arrhythmia (n = 31) or multiple appropriate shocks from an implantable cardioverter-defibrillator (ICD) (n = 4). Asymptomatic patients with inducible arrhythmia underwent electrophysiologic (EP)-guided therapy. When ventricular tachycardia (VT)/ventricular fibrillation (VF) inducibility was not prevented, or in case of HQ intolerance, an ICD was placed. RESULTS: Hydroquinidine prevented VT/VF inducibility in 76% of asymptomatic patients who underwent EP-guided therapy. Syncope occurred in two of the 21 patients who received long-term (17 +/- 13 months) HQ therapy (1 syncope associated with QT interval prolongation and 1 unexplained syncope associated with probable noncompliance). In asymptomatic patients who received an ICD (n = 10), one appropriate shock occurred during a follow-up period of 13 +/- 8 months. In patients with multiple ICD shocks, HQ prevented VT/VF recurrence in all cases during a mean follow-up of 14 +/- 8 months. CONCLUSIONS: Hydroquinidine therapy prevented VT/VF inducibility in 76% of asymptomatic patients with BrS and inducible arrhythmia, as well as VT/VF recurrence in all BrS patients with multiple ICD shocks. These preliminary data suggest that preventive treatment by HQ may be an alternative strategy to ICD placement in asymptomatic patients with BrS and inducible arrhythmia.

Adolescent↗
PubMed2004

[Typical and atypical atrial flutters].

Definitions, classification, surface electrocardiographic characterisitics, risk for stroke and treatments. Atrial flutters are macro-reentrant circuits originated from both right and left atria. They have been classified in typical and atypical based on their cavo-tricuspid isthmus-dependence. Typical atrial flutter comprises counterclockwise and clockwise isthmus-dependent atrial flutter located within the right atrium. Atypical atrial flutters are composed by non-isthmus-dependent right atrial flutter and left atrial flutter. Typical atrial flutter represents at least 90% of all flutters, and has usually a counterclockwise pattern. Ablation is a potential definitive therapy for atrial flutter. However, successful procedures as well as complications rates are different depending of the location of the circuit. There are now evidences for risk of stroke related to atrial flutter, although epidemiological studies have not been conducted yet. Therefore, prevention of such complications using anti-thrombotic should be performed as done for atrial fibrillation.

Atrial Flutter↗
PubMed2003

A rare localization in right-sided endocarditis diagnosed by echocardiography: a case report.

BACKGROUND: Right-sided endocarditis occurs predominantly in intravenous drug users, patients with pacemakers or central venous lines and with congenital heart diseases. The vast majority of cases involve the tricuspid valve. CASE PRESENTATION: A case of a 31-year-old woman with intravenous drug abuse who had a right-sided vegetation attached to the muscular bundle of the right ventricle is presented. Transthoracic echocardiography revealed a vegetation in the right ventricular outflow tract. Transesophageal echocardiography clearly showed that the 1.8 cm vegetation was not adherent to the pulmonary valve but attached to a muscular bundle. CONCLUSIONS: Our case points to an unusual location of right-sided endocarditis in intravenous drug users. It confirms that TTE remains an easy and highly sensitive first-line examination for the diagnosis of right-sided endocarditis.

Adult↗
PubMed2003

Fibrosis of the left atria during progression of heart failure is associated with increased matrix metalloproteinases in the rat.

OBJECTIVES: The purpose of this study was to determine the pathogenic factors and molecular mechanisms involved in fibrosis of the atria. BACKGROUND: Fibrosis is an important component of the pathophysiology of atrial fibrillation, especially when the arrhythmia is associated with heart failure (HF) or atrial dilation. METHODS: We used a rat model of myocardial infarction (MI) complicated by various degrees of left ventricular dysfunction and atrial dilation to study fibrosis and matrix metalloproteinase (MMP) activity in the left atrial (LA) myocardium by means of histologic, Western blot, zymographic, and immunohistologic techniques. RESULTS: Three months after surgical ligature of the left coronary artery, 27 rats had a large MI, 12 were in mild HF, and 15 in severe HF. Both groups had LA enlargement at the echocardiography. Masson's trichrome and picrosirius staining of tissue sections revealed marked fibrosis at the periphery of trabeculae and also surrounding myolytic myocytes, in both mild and severe HF. In mild HF, the activity and expression of the matrilysin MMP-7 were increased (122%), whereas in severe HF, both MMP-7 (211%) and the gelatinase MMP-2 (187%) were up-regulated. There were no changes in the expression or activity of MMP inhibitors, TIMP-1, -2, and -4. Immunostaining of cryosections showed that MMP-2 was present in the interstitial spaces, whereas MMP-7 accumulated in myolytic myocytes. CONCLUSIONS: Hemodynamic overload of the atria is an important pathogenic factor of fibrosis; MMP-7 appears to be involved in the early stage of this tissue remodeling process.

Animals↗
PubMed2003

The long QT interval is not only inherited but is also linked to cardiac hypertrophy.

This review focuses on the molecular determinants of the duration of the QT interval as measured on by electrocardiography in normal subjects and during cardiac hypertrophy and failure. (a) In control conditions, on a single cell, the shape and duration of the action potential is the result of a balance between different ion currents which in turn were determined by the number of functional channels. On multicellular preparations the QT duration also represents the repolarization time; nevertheless it is modified by the transmural gradients. On body-surface electrocardiography the duration of the QT interval depends also of an additional factor: the spatial three-dimensional projection of the electrical waves vectors, which makes any determination of the epicardial dispersion by measuring QT interval dispersion questionable. (b) The enhanced action potential duration is well documented in cardiac hypertrophy and heart failure and is usually caused by a reduction in outward current densities in most of the species except mice. Among these currents I(tO) is the most frequently altered, especially in humans. Such an altered current density is caused by a diminished expression of the genes encoding either the ion channel subunits or regulatory proteins, such as KChIP2. In addition, hypertrophy modifies or even reverses the transmural gradient. In human and rats hypertensive cardiopathy is associated with a prolongation of the QT interval duration. The reduction in I(tO) is likely to be adaptive; it participates in the slowing of the cardiac cycle and reflects the fetal genetic reprogramming. Recent data also suggest that a reduction in the transient outward K(+) current density triggers protein synthesis through an activation of the calcineurin pathways. Thus a prolongation of the QT interval is not only inherited or drug-induced; it is also an essential component of the adaptive process in chronic mechanical overload. It is fundamentally incorrect to measure QT dispersion on a surface electrocardiography, but the mean QT interval may provide information concerning the progression of the disease, just as, and with the same restrictions, in the case of the quantification of V(max).

Animals↗
PubMed2003

Decreased nocturnal standard deviation of averaged NN intervals. An independent marker to identify patients at risk in the Brugada Syndrome.

AIMS: Risk-stratification of asymptomatic Brugada Syndrome (BS) patients remains a key-issue. A typical spontaneous BS-ECG pattern and ventricular tachycardia (VT)/ventricular fibrillation (VF) inducibility are two recognized risk markers. The aim of the study was to identify additional risk markers in asymptomatic BS. METHODS AND RESULTS: We have compared Holter recordings in symptomatic and in asymptomatic patients with BS. Heart rate variability (HRV), QT-interval rate-dependence and ST-segment elevation (ST-SE) were analysed. The study population included 47 BS patients (M=36, mean age=45+/-13 years) with a malignant ventricular arrhythmia in 11 cases, an unexplained syncope in 10 cases and no symptoms in the remaining 26 cases. A typical spontaneous BS-ECG was present in 21 cases and a drug-induced BS-ECG in 26 cases. A downward trend of the time domain variables of HRV was observed. During the nocturnal period, standard deviation (SD) of the 5min averaged NN intervals (SDANN) (46+/-13 vs 57+/-18ms, P=0.02) and ultra low frequency component (3287+/-2312 vs 5030+/-3270 ms(2), P=0.04) were significantly lower in symptomatic versus asymptomatic patients. In contrast, no difference was found in QT-interval rate dependence and in ST-SE. At multivariate logistic regression, VT/VF inducibility, typical spontaneous BS-ECG and a decreased nocturnal SDANN were associated with arrhythmic events (P=0.003). CONCLUSIONS: A decreased nocturnal SDANN was an independent marker of arrhythmic events in these BS patients.

Adult↗