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Background Uncontrolled studies have shown that short atrioventricular delay dual chamber pacing reduces outflow tract obstruction in hypertrophic obstructive cardiomyopathy. Although the exact mechanism of this beneficial effect is unclear, this seems a promising potential new treatment for hypertrophic obstructive cardiomyopathy. Method In order to evaluate the impact of pacing therapy, we performed a randomized multicentre double-blind crossover (pacemaker activated vs non activated) study to investigate modification of echocardiography, exercise tolerance, angina, dyspnoea and quality of life in 83 patients with a mean age of 53 (range 22–87) years with symptoms refractory or intolerant to classical drug treatment. Results After 12 weeks of activated or inactivated pacing, independent of which phase was first, the pressure gradient fell from 59±36 mmHg to 30±25 mmHg ( P

The rodent model of myocardial infarction (MI) is extensively used in heart failure studies. However, long-term follow-up of echocardiographic left ventricular (LV) function parameters such as the myocardial performance index (MPI) and its ratio with the fractional shortening (LVFS/MPI) has not been validated in conjunction with invasive indexes, such as those derived from the conductance catheter (CC). Sprague-Dawley rats with left anterior descending coronary artery ligation (MI group, n = 9) were compared with a sham-operated control group ( n = 10) without MI. Transthoracic echocardiography (TTE) was performed every 2 wk over an 8-wk period, after which classic TTE parameters, especially MPI and LVFS/MPI, were compared with invasive indexes obtained by using a CC. Serial TTE data showed significant alterations in the majority of the noninvasive functional and structural parameters (classic and novel) studied in the presence of MI. Both MPI and LVFS/MPI significantly ( P < 0.05 for all reported values) correlated with body weight ( r = −0.58 and 0.76 for MPI and LVFS/MPI, respectively), preload recruitable stroke work ( r = −0.61 and 0.63), LV end-diastolic pressure (LVEDP) ( r = 0.82 and −0.80), end-diastolic volume ( r = 0.61 and −0.58), and end-systolic volume ( r = 0.46 and −0.48). Forward stepwise linear regression analysis revealed that, of all variables tested, LVEDP was the only independent determinant of MPI ( r = 0.84) and LVFS/MPI ( r = 0.83). We conclude that MPI and LVFS/MPI correlate strongly and better than the classic noninvasive TTE parameters with established, invasively assessed indexes of contractility, preload, and volumetry. These findings support the use of these two new noninvasive indexes for long-term analysis of the post-MI LV remodeling.

Aims Atrioventricular synchronous pacing exerts beneficial effects, including reduction of left ventricular outflow tract gradients, in patients with hypertrophic obstructive cardiomyopathy. The Pacing in Cardiomyopathy study was initiated to explore the effects of pacing in a double-blind randomized crossover fashion. The aims were to ascertain the beneficial effects of pacing in a controlled study and to rule out a placebo effect by pacing. This paper deals with the outcome of pacing on quality of life during 1 year of follow-up. Methods Quality of life was evaluated with the Karolinska questionnaire, validated for patients paced for bradyarrhythmias and ischaemic heart disease. Drug-refractory patients with hypertrophic obstructive cardiomyopathy were recruited for the study and after a temporary pacing procedure implanted with permanent pacemakers. Patients were randomized to two study arms defining the sequence of pacemaker programming. In one arm the pacemaker was inactive, in the other active. After 3 months the pacemaker was reprogrammed to the alternate mode and a further 3 months followed. After this period subsequent pacemaker programming corresponded to the mode preferred by the patient. A last assessment was made 1 year after baseline examinations. Results Eighty patients completed the first crossover period and 75 completed the full 1 year of follow-up. Active pacing induced significant quality of life improvements, in the order of 9–44%, regardless of programming sequence. Discontinuation of pacing after a first active period resulted in the return of symptoms. Fourteen patients requested early reprogramming after having been programmed to inactive pacing after a first period of active pacing. Seventy-six patients preferred active pacing after the crossover period. A further 6 months of pacing induced progressive improvement in symptoms already favourably influenced. Conclusion Atrioventricular synchronous pacing has a profound beneficial effect on most domains of quality of life in patients with hypertrophic obstructive cardiomyopathy refractory to drug treatment.

Background The therapeutic options for hypertrophic obstructive cardiomyopathy (HOCM) classically include medical treatment with beta-blockers and calcium antag-onists or myectomy–myotomy as a surgical possibility for refractory cases. The observation that pacemaker activation of the heart in HOCM reduces the subaortic gradient is well known but less well investigated. Methods Eighty-three patients (33 female and 50 male) mean age 53 (18–82) years, with symptoms refractory to drug treatment and a resting gradient above 30 mmHg, who responded favourably to temporary pacing, were included in this prospective study and had a pacemaker (DDD) implanted. After an initial double-blind crossover phase of 6 months, patients were reinvestigated at 12 months and followed for a mean of 36 months. Results As observed during a screening investigation, the obstruction was significantly reduced from 72±35 mmHg to 29±24 mmHg ( P

Figure 2 Standard chest CT scan after contrast media injection. A transverse section (1.2 mm thickness) at the aortic root level showing circumferential pericardial calcification (arrow) and right pleural effusion (*). B 3D reconstruction of the heart and great vessels (anterior view) demonstrating calcifications of the pericardium (in yellow) covering most of the antero-lateral wall of the left ventricle. A B

Objective: To define therapeutic strategy for management of patients with ischemic stroke due to a high probability of paradoxical embolism through a Patent Foramen Ovale (PFO). Methods: Since 1988 all consecutive patients with cerebrovascular events and PFO from the Stroke Registry of our population-based primary-care center are prospectively studied and followed. Since 1992, among 118 patients with cryptogenic embolic brain infarct or transient ischemic attack (TIA) and PFO, 32 consecutive patients younger than 60 years who presented at least two of the following criteria were admitted for surgery: history of Valsalva strain before stroke (11); multiple clinical events (13); multiple infarcts on brain Magnetic Resonnance Imaging (MRI) (15); atrial septal aneurysm (ASA) (16); large right-to-left shunt (\ 50 microbubbles) (12). Results: Operative time 135%9 33%. CPB time 34%914%. Aortic crossclamping time 16%96%. Post-operative bleeding 4859 170 ml. No homologous blood transfusion required. No neurological, cardiac or renal complications. All patients were followed-up corresponding to a cumulative time of 601 patient-months. This revealed no reccurent vascular events nor silent new brain lesions on brain MRI. Systematic simultaneous contrast Trans Esophageal Echocardiography (TEE)—Trans Cranial Doppler showed a small residual interatrial shunt in two patients. Conclusion: Surgical closure of a patent foramen ovale can be accomplished with very low morbidity and reduce efficently the risk of stroke recurrence. It seems to be the option of choice in selected patients with a higher (\ 1.5%: year) risk of stroke recurrence. © 1997 Elsevier Science B.V.

All studies concerning the detection of patent foramen ovale (PFO) have compared transthoracic or transesophageal echocardiography (c-TEE) to transcranial Doppler ultrasound after contrast injection (c-TCD), but combining both techniques in the search of PFO has received no consideration. Our study aims to substantiate this claim in 37 patients with cryptogenic stroke. It includes two protocols for the detection of PFO to assess the complementarity of c-TCD and c-TEE performed simultaneously or separately. Firstly, we used a standardized protocol, performing c-TCD alone. Secondly, we used a standardized and a simultaneous protocol which associated c-TCD with c-TEE. When c-TCD and/or c-TEE found right-to-left shunts, they were classified as: minimal, intermediate and massive. c-TCD revealed all PFO detected by c-TEE in 24 patients out of 37 (65%). Furthermore, c-TCD was positive for a PFO in 5 other patients whereas c-TEE was negative. The degree of right-to-left interatrial shunting varied according to the protocol: c-TCD performed alone found 15 massive, 4 intermediate and 5 minimal shunts whereas 10, 9 and 5, respectively, were detected by c-TCD when it was combined with c-TEE. In contrast, c-TEE revealed 8 massive, 8 intermediate and 8 minimal shunts. c-TCD can identify minimal shunts missed by c-TEE and could be more relevant to detect massive shunts, particularly when not performed simultaneously with c-TEE because no sedation is required for c-TCD alone as opposed to c-TEE: thus patients are more cooperative and produce a better Valsalva strain. c-TEE confirms pulmonary shunts suspected by c-TCD and determines the morphologic characteristics of the interatrial septum. While previous studies opposed c-TEE against c-TCD for the detection of a PFO, we think that both techniques are complementary and that it is interesting to associate them, particularly when they are deferred, to increase the ability of detecting PFO and to specify the degree of right-to-left shunting.

The results of several large multicenter CMR studies were reported in 2012, thus, constantly corroborating the evidence on CMR performance. In this review, we present results of the MR-IMPACT programme and the CE-MARC study, which demonstrated the superiority of perfusion-CMR over gated SPECT for the workup of suspected CAD, the currently available data from the European CMR registry, comprising almost 30,000 patients from 57 participating centers in 15 European countries, and finally, the results of the Advisa-MRI study, which documented the safety of a MRI-compatible pacemaker system. These large trials and others set the basis for the recommendations in the new European guidelines on heart failure to use CMR as a first line method if echocardiographic quality is inadequate or the etiology of heart failure is unclear.

The present review provides a selected choice of clinical research in the field of interventional cardiology, electrophysiology and cardiac imaging. We also focused on the new guidelines published by the European society of cardiology in 2010 (revascularization, atrial fibrillation and device therapy in heart failure).

The problem of stroke of unknown origin is still unsolved. Since the report of the high prevalence of patent foramen ovale (PFO) in young stroke populations, paradoxical embolism has been suggested as

Echocardiography is the preferred initial noninvasive test to assess heart muscle and heart valves. Cardiac MRI has a unique capacity to directly characterise myocardial tissue with specific imaging sequences and late enhancement pattern after gadolinium injection, and has a specific role in the diagnosis of cardiomyopathies. In valvular heart diseases, cardiac MRI precisely measures the severity of aortic or pulmonary regurgitation. In pericardial heart diseases, and specifically when constrictive pericarditis is suspected, cardiac MRI and/or CT are useful to look for pericardial thickening. Cardiac CT and MRI are very rapidly developing techniques in cardiology; the use of these expensive techniques must follow the currently accepted indications in order to be integrated in a rational diagnosis process in clinical practice.

Systemic amyloidosis with cardiac involvement may clinically be suspected in the presence of heart failure or arrhythmia of unknown origin. Herein two cases of cardiac amyloidosis are described with a clinical presentation of heart failure refractory to usual treatment. The key role of echocardiography in the diagnosis and prognosis evaluation of cardiac amyloidosis is discussed. A treatment targeted against the generation of amyloid fibril should ideally be initiated before apparition of heart failure.

Terminal heart failure can be the cause or the result of major dysfunctions of the organisms. Although, the outcome of the natural history is the same in both situations, it is of prime importance to differentiate the two, as only heart failure as the primary cause allows for successful mechanical circulatory support as bridge to transplantation or towards recovery. Various objective parameters allow for the establishment of the diagnosis of terminal heart failure despite optimal medical treatment. A cardiac index2.0 l/min, and a mixed venous oxygen saturation60%, in combination with progressive renal failure, should trigger a diagnostic work-up in order to identify cardiac defects that can be corrected or to list the patient for transplantation with/without mechanical circulatory support.

Aims: Mitral valve prolapse is a common source of severe mitral regurgitation in Western countries. Three-dimensional echocardiography can provide views of the entire valve, allowing a complete assessment of the valve leaflets and commissures. It has the potential to precisely locate and quantify mitral valve prolapse. Methods and results: Between January 1997 and December 2000, 91 patients with severe mitral regurgitation due to mitral valve prolapse underwent a transesophageal echocardiography with three-dimensional reconstruction of the mitral valve as part of their pre-operative work-up. The location and extent of the prolapse by echo was compared to the surgical status. The volume of prolapsing leaflet was calculated and compared to the volume of resected tissue whenever a repair was attempted. There was an excellent correspondence between the echographic localization of the prolapse and surgical inspection, and between the volume of prolapsing and surgically resected tissue ( r = 0.94, p

The therapeutic options for hypertrophic obstructive cardiomyopathy (HOCM) classically include medical treatment with beta-blockers and calcium antagonists or myectomy-myotomy as a surgical possibility for refractory cases. The observation that pacemaker activation of the heart in HOCM reduces the subaortic gradient is well known but less well investigated.Eighty-three patients (33 female and 50 male) mean age 53 (18-82) years, with symptoms refractory to drug treatment and a resting gradient above 30 mmHg, who responded favourably to temporary pacing, were included in this prospective study and had a pacemaker (DDD) implanted. After an initial double-blind crossover phase of 6 months, patients were reinvestigated at 12 months and followed for a mean of 36 months.As observed during a screening investigation, the obstruction was significantly reduced from 72 +/- 35 mmHg to 29 +/- 24 mmHg (P0.01) when the pacemaker was on, while no major effect was seen during the sham phase. The effect was persistent at 1 year with a remaining resting gradient of 28 +/- 24 mmHg. In parallel, we documented an improvement in functional capacity, according to the NYHA classification and by quality of life analysis, and a significant improvement in dyspnoea and angina. Exercise on treadmill improved only in patients with reduced initial tolerance (8 min). During the mean follow-up of 36 months, 65 patients remained on pacing alone, with eight patients having additional AV-node ablation and five patients finally having surgery.This controlled multicentre study shows that pacemaker treatment is an option for HOCM patients; it is inoffensive and does not exclude alternative methods, but satisfies 79% of patients beyond 3 years.

Atrioventricular synchronous pacing exerts beneficial effects, including reduction of left ventricular outflow tract gradients, in patients with hypertrophic obstructive cardiomyopathy. The Pacing in Cardiomyopathy study was initiated to explore the effects of pacing in a double-blind randomized crossover fashion. The aims were to ascertain the beneficial effects of pacing in a controlled study and to rule out a placebo effect by pacing. This paper deals with the outcome of pacing on quality of life during 1 year of follow-up.Quality of life was evaluated with the Karolinska questionnaire, validated for patients paced for bradyarrhythmias and ischaemic heart disease. Drug-refractory patients with hypertrophic obstructive cardiomyopathy were recruited for the study and after a temporary pacing procedure implanted with permanent pacemakers. Patients were randomized to two study arms defining the sequence of pacemaker programming. In one arm the pacemaker was inactive, in the other active. After 3 months the pacemaker was reprogrammed to the alternate mode and a further 3 months followed. After this period subsequent pacemaker programming corresponded to the mode preferred by the patient. A last assessment was made 1 year after baseline examinations.Eighty patients completed the first crossover period and 75 completed the full 1 year of follow-up. Active pacing induced significant quality of life improvements, in the order of 9-44%, regardless of programming sequence. Discontinuation of pacing after a first active period resulted in the return of symptoms. Fourteen patients requested early reprogramming after having been programmed to inactive pacing after a first period of active pacing. Seventy-six patients preferred active pacing after the crossover period. A further 6 months of pacing induced progressive improvement in symptoms already favourably influenced.Atrioventricular synchronous pacing has a profound beneficial effect on most domains of quality of life in patients with hypertrophic obstructive cardiomyopathy refractory to drug treatment.

Assessment of right ventricular volume and function is important in many clinical settings involving heart or lung disease. However, the complexity of the right ventricular anatomy has prevented accurate volume determination by two-dimensional echocardiography. In the present study, 5 models incorporating standard echocardiographic views, were used to determine right ventricular volume in 10 human subjects. Two models were contingent on the true crescentic appearance of the right ventricle, whereas the remaining 3 calculated the right ventricular volume as a pyramid, an ellipsoid or other tapering geometrical figures, respectively. Subsequently, echocardiographic right ventricular volumes were compared to magnetic resonance imaging derived volumes. Correlation analysis and agreement measurement between the echocardiographic and magnetic resonance end-diastolic volume were performed in 10 out of 10 subjects and in 9 out of 10 subjects for the end-systolic volume. The 2 crescentic models resulted in the most reliable estimation of right ventricular volume. Those findings suggest that models based on right ventricular anatomical landmarks are feasible and should be preferred in echocardiographic studies.

Cardiac pacing using the apex of the right ventricle as site of excitation induces asynchronous contraction between the right ventricle and the left ventricle as well as inversion of the normal left ventricular activation sequence. These two phenomena are responsible for alteration of septal kinetics and overall contractility. It has recently been demonstrated that these alterations can be used to advantage to reduce the degree of subaortic obstruction of patients suffering from hypertrophic and obstructive cardiomyopathy, and to improve their exercise tolerance. Using an opposite approach, consisting of reducing the degree of asynchronous contraction related to the presence of intraventricular conduction disorders, while optimizing atrioventricular synchronism, new pacing methods have recently been able to improve cardiac output and functional tolerance of some patients suffering from dilated cardiomyopathy. Although cardiac pacing can now be considered to be an alternative a surgery for the treatment of refractory forms of hypertrophic and obstructive cardiomyopathy, it still constitutes a research technique in the field of dilated cardiomyopathy.

Uncontrolled studies have shown that short atrioventricular delay dual chamber pacing reduces outflow tract obstruction in hypertrophic obstructive cardiomyopathy. Although the exact mechanism of this beneficial effect is unclear, this seems a promising potential new treatment for hypertrophic obstructive cardiomyopathy.In order to evaluate the impact of pacing therapy, were performed a randomized multicentre double-blind cross-over (pacemaker activated vs non activated) study to investigate modification of echocardiography, exercise tolerance, angina, dyspnoea and quality of life in 83 patients with a mean age of 53 (range 22-87) years with symptoms refractory or intolerant to classical drug treatment.After 12 weeks of activated or inactivated pacing, independent of which phase was first, the pressure gradient fell from 59 +/- 36 mmHg to 30 +/- 25 mmHg (P0.001) with active pacing. Exercise tolerance improved by 21% in those patients who at baseline tolerated less than 10 min of Bruce protocol; symptoms of dyspnoea and angina also improved significantly from NYHA class 2.4 to 1.4 and 1.0 to 0.4, respectively (P0.007). Quality of life assessment with a validated questionnaire objectivated the subjective improvement.Pacemaker therapy is of clinical and haemodynamic benefit for patients with hypertrophic obstructive cardiomyopathy, left ventricular outflow gradient at rest over 30 mmHg who are symptomatic despite drug treatment.

Our understanding of cardiac failure has greatly changed over the last 15 years. Left ventricular diastolic dysfunction, which is now recognised as one of the primary causes of certain types of cardiac failure (1). Abnormal left ventricular diastolic function is the common determinant and indeed the earliest sign of all chronic left ventricular failures whether systolic left ventricular dysfunction is associated with it or not (2). In this paper, we review the basis of diastolic dysfunction and its impact on diagnosis and treatment of cardiac failure.

Advancing The Standard (ATS) Medical (ATS Medical Inc., Minneapolis, MN) is a new mechanical bileaflet valve, composed of pyrolitic carbon. The aim of this study was to define in a blinded manner the Doppler echocardiographic characteristics of normally functioning ATS Medical prostheses with respect to their size. Forty consecutive patients (29 men, mean age 58 +/- 13 years), clinically stable, and without evidence of valve dysfunction, were studied from 1993 to 1995. Doppler echocardiography was performed at least 3 months after valve replacement with ATS Medical valves (5 n degrees 21, 8 n degrees 23, 12 n degrees 25, 10 n degrees 27, 5 n degrees 29). Maximum and mean transprosthetic pressure gradients were calculated by the simplified Bernoulli equation. Functional valve surface area was assessed by the continuity equation using the external diameter of the prostheses to calculate the subaortic surface area. The Doppler velocity index was obtained by the ratio of subaortic and transaortic velocities and the performance index was calculated dividing the effective orifice area by the actual orifice area. For the most commonly used aortic valve (25 mm), the maximum pressure gradient was 17 +/- 8 mmHg, the mean gradient 11 +/- 4 mmHg, the functional surface area 2.2 +/- 0.4 cm2, the Doppler velocity index 0.44 +/- 0.07, and the performance index 0.68 +/- 0.11. This study provides the normal range for Doppler hemodynamic characteristics of the various sizes of the ATS valve.

Patent foramen ovale (PFO) is more common in patients with stroke than in matched controls, but the stroke mechanism and late prognosis are not well known. We studied features, coexisting causes, and recurrences of stroke in 140 consecutive patients (mean age 44 +/- 14 years) with stroke and PFO admitted to a population-based primary-care center. We selected the patients from 340 patients (41%) agedor = 60 years with acute stroke. The initial event was brain infarction in 118 patients (84%) and TIA in 22 (16%). Intracranial embolic occlusions were present on angiography or transcranial Doppler in most patients admitted within 12 hours of onset, whereas a venous source was clinically apparent in only six patients (5.5%). Pulmonary embolism, Valsalva maneuver at onset, and coagulation abnormalities were rare, but one-fourth of the patients had an interatrial septum aneurysm (ISA) that coexisted with PFO. An alternative cause of stroke was present in only 22 patients (16%), usually cardiac (atrial fibrillation, severe mitral valve prolapse, akinetic left ventricular segment). During a mean follow-up of 3 years, the stroke or death rate was 2.4% per year, but only eight patients had a recurrent infarct (1.9% per year). This low rate of recurrence contrasted with the severity of initial stroke, which left disabling sequelae in one-half the patients. Multivariate analysis showed that interatrial communication, a history of recent migraine, posterior cerebral artery territory infarct, and a coexisting cause of stroke were associated with recurrence, whereas ISA and treatment type (coagulant or antiaggregant therapy, surgical closure of PFO) were not. However, given the low number of events, these findings must be taken with caution. In conclusion, our study shows that stroke associated with PFO with or without ISA is not commonly due to a coexisting cause of stroke. It is usually embolic, although a definite source cannot often be demonstrated. The presenting stroke is often severe, but recurrence is uncommon. The demonstration of factors associated with a higher risk of recurrence in subgroups of patients is critical for the long-term management of these patients.

Pacing reduces the sub-aortic pressure gradient in hypertrophic obstructive cardiomyopathy. This phenomenon was described long ago but only recently, with the development of sophisticated pacemakers, has it become possible to use pacemakers for the long term treatment of this disease. The acute hemodynamic improvement with pacemaker treatment is well documented. The reason for this acute and chronic improvement is of multiple origin. Pacing modulates the activation sequence of the left ventricle, reduces contractility, reduces subaortic flow velocities, influences mitral valve movement and leads to remodeling of the ventricle in the long term. All these factors together explain the clinical and hemodynamic improvement in patients suffering from hypertrophic obstructive cardiomyopathy.

Up until recently, the first-line treatment of obstructive hypertrophic cardiomyopathy was pharmacological and surgical in refractory cases. However, the immediate beneficial effect of a cardiac pacing on infra-aortic obstruction has been known for many years. The development of sophisticated two-chamber pacemakers and their use in patients with obstructive hypertrophic cardiomyopathy has confirmed their beneficial effect both in terms of haemodynamic and clinical parameters. There appears to be many reasons for this advantageous effect and only some of them have been elucidated, including alteration of the activation sequence of the left ventricle secondary to apical ectopic electrical activation and reduction of the contact time of the mitral valve with the proximal septum and, in the long term, ventricular remodelling secondary to release of the outflow obstruction. The increasing number of publications reporting a beneficial effect of two-chamber pacemakers in these patients justifies consideration of this approach in all patients refractory to drug therapy.

Subaortic pressure gradient in hypertrophic obstructive cardiomyopathy (HOCM) is the consequence of a dynamic obstruction of the left ventricular outflow tract linked to the presence of a hypertrophied septum. We tried to induce an altered septal motion electrically by physiologic pacing. We studied 8 patients (6 men, 2 women, mean age 60 +/- 13 years) with symptomatic HOCM, resistant to optimal drug treatment. During a hemodynamic study, dual chamber pacing significantly reduced the preexistent subaortic pressure gradient, from 69 +/- 39 to 34 +/- 26 mm Hg (p less than 0.004), without concomitant reduction of aortic pressure or cardiac output. This reduction was dependent upon a optimized AV interval. A dual chamber pacemaker (PM) was then implanted and programmed to VDD mode and optimized AV delay interval (50-90 ms), warranting full ventricular capture. The follow-up of 3 to 30 months showed a significant reduction of both angina (from NYHA class 3 to 1: p less than 0.009) and dyspnea (from 3 to 2: p less than 0.03). An echo-doppler study in 6 patients proved the persistence of the beneficial effect of the stimulation by showing a significant reappearance of the subaortic pressure gradient after switching off the PM, from 44 +/- 29 in VDD pacing mode to 77 +/- 44 mm Hg (p less than 0.02). We conclude that atrial synchronized ventricular pacing, together with an optimized AV interval, significantly reduces the outflow gradient and improves symptoms in patients with HOCM. An altered ventricular activation sequence with late septal activation is suspected to be the mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

The recording of the velocity of tricuspid valve regurgitation by continuous wave Doppler enables the calculation of the instantaneous systolic pressure gradient between the right ventricle and right atrium. As right atrial pressure is relatively constant, the rate of acceleration of the regurgitant jet reflects the quality of the rise in pressure in the right ventricle in early diastole, and therefore right ventricular contractility. The authors studied 3 Doppler parameters of the rate of velocity increase of the tricuspid regurgitation; the maximum rate of acceleration (dV/dt max), the maximum derivative of the pressure (dP/dt max) and the mean rate of increase in pressure (T). The interobserver variability of these indices is low (r greater than 0.96); reproducibility is good in patients with sinus rhythm but mediocre in atrial fibrillation. The comparison of the Doppler indices with the right ventricular isotopic fraction in 26 patients with tricuspid regurgitation showed a good correlation (dV/dt max, r = 0.79, p less than 0.0001; dP/dt max, r = 0.69, p less than 0.0001; T, r = 0.60, p = 0.0012). These results show that right ventricular systolic function can be evaluated by continuous wave cardiac Doppler by recording the spectral envelope of tricuspid regurgitation.

Over a six months' period we prospectively studied the prevalence of patent foramen ovale (PFO) in patients under 50 years of age admitted for cerebral infarction as assessed by cerebral computed tomography. The study recruited 16 patients (9 male, 7 female, mean age 39 +/- 10 years). Before the contrast study, 5 patients had other identifiable sources of stroke after neurologic investigations and 2-D echocardiography with color-Doppler, whereas 11 had no precise origin. The overall prevalence was 50% with 8 PFO demonstrated, 6 during normal breathing and two during a coughing test. All were in the sub-group of 11 patients without a predetermined source of stroke (prevalence 73%) and in 83% of patients aged under 40. In accordance with the literature, we found a high prevalence of PFO in the ischemic cerebral infarction population aged under 50 years and without another possible source of stroke; this prevalence is higher in patients under 40 years old. This observation confirms the suspicion of paradoxical embolism in these cases.

Doppler echocardiography is a reliable non-invasive method of following up patients with prosthetic heart valves. Transthoracic M mode and two-dimensional echo allow evaluation of the movement of the mobile element of the prosthesis and of the size of the cardiac chambers. Doppler studies (transprosthetic pressure gradient, valve surface area, trans- and periprosthetic regurgitation) give an indication of the hemodynamic profile of the prosthesis. Transesophageal echocardiography is especially useful when there are abnormalities suggestive of prosthetic valve dysfunction (fever, systemic embolism, clinical symptoms, haemolysis...).

The vitamin D3 and nicotine (VDN) model is one of isolated systolic hypertension (ISH) in which arterial calcification raises arterial stiffness and vascular impedance. The effects of VDN treatment on arterial and cardiac hemodynamics have been investigated; however, a complete analysis of ventricular-arterial interaction is lacking. Wistar rats were treated with VDN (VDN group, n = 9), and a control group ( n = 10) was included without the VDN. At week 8, invasive indexes of cardiac function were obtained using a conductance catheter. Simultaneously, aortic pressure and flow were measured to derive vascular impedance and characterize ventricular-vascular interaction. VDN caused significant increases in systolic (138 ± 6 vs. 116 ± 13 mmHg, P < 0.01) and pulse (42 ± 10 vs. 26 ± 4 mmHg, P < 0.01) pressures with respect to control. Total arterial compliance decreased (0.12 ± 0.08 vs. 0.21 ± 0.04 ml/mmHg in control, P < 0.05), and pulse wave velocity increased significantly (8.8 ± 2.5 vs. 5.1 ± 2.0 m/s in control, P < 0.05). The arterial elastance and end-systolic elastance rose significantly in the VDN group ( P < 0.05). Wave reflection was augmented in the VDN group, as reflected by the increase in the wave reflection coefficient (0.63 ± 0.06 vs. 0.52 ± 0.05 in control, P < 0.05) and the amplitude of the reflected pressure wave (13.3 ± 3.1 vs. 8.4 ± 1.0 mmHg in control, P < 0.05). We studied ventricular-arterial coupling in a VDN-induced rat model of reduced arterial compliance. The VDN treatment led to development of ISH and provoked alterations in cardiac function, arterial impedance, arterial function, and ventricular-arterial interaction, which in many aspects are similar to effects of an aged and stiffened arterial tree.

The purpose of the present work was to study the effect of a methionine-enkephalin analogue (FK 33-824) on glucose tolerance in man. Groups of 5 to 8 normal subjects were given a 0.5 mg im injection of the drug or placebo just before a 100 g oral glucose load or a 0.5 g/kg iv glucose load. In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. This effect was not observed when glucose was given iv in another group of 5 subjects in whom the significant blunting of the insulin response was accompanied by a significant decrease in glucose tolerance. These observations demonstrate that in man, enkephalin produces a decrease in insulin secretion in response to both oral and iv glucose loads. The absence of any marked impairment in glucose tolerance in the oral test in spite of the decreased insulin response suggests that enkephalin might have an additional effect in delaying glucose absorption.

It has been suggested that the shape of the normalized time-varying elastance curve [En( tn)] is conserved in different cardiac pathologies. We hypothesize, however, that the En( tn) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats ( n = 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) ( n = 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the En( tn) derived. Slopes of En( tn) during the preejection period (αPEP), ejection period (αEP), and their ratio (β = αEP/αPEP) were calculated, together with the characteristic decay time during isovolumic relaxation (τ) and the normalized elastance at end diastole (Eminn). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (−33%), ejection fraction (−40%), and stroke volume (−30%) ( P < 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 ± 0.31 mmHg/μl (CTRL) to 0.34 ± 0.11 mmHg/μl (MI) ( P < 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods ( P < 0.05). The slope of En( tn) during the αPEPand β were significantly altered after MI ( P < 0.05). Furthermore, τ and end-diastolic Eminnwere both significantly augmented in the MI group. We conclude that the En( tn) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept.