[Saw tooth cardiomyopathy: How to better diagnose?] / Saw tooth cardiomyopathy : comment mieux faire le diagnostic ?

With the increasing use of cardiac MRI, several cases were described as "sawtooth cardiomyopathy" or "tiger heart". The pathological aspects of these rare forms of myocardial dysplasia, frequently assimilated to non-compaction of the left ventricle, and its prognostic implications remain unclear. We present a case of "sawtooth cardiomyopathy" in a patient with a transient ischemic attack. This article aims to determine, with the other clinical cases in the literature, the MRI and echocardiography criteria for the diagnosis of this cardiomyopathy. Sawtooth cardiomyopathy is probably under diagnosed and deserves to be better known.

[Pathophysiology of right ventricular hemodynamics]. / Physiopathologie hémodynamique du ventricule droit.

The right ventricle (RV) plays a key role in the maintenance of an adequate cardiac output whatever the demand, and thus contributes to the optimization of the ventilation/perfusion ratio. The RV has a thin wall and it buffers the physiological increases in systemic venous return without causing a deleterious rise in right atrial pressure (RAP). The RV is coupled to the pulmonary circulation which is a low pressure, low resistance, high compliance system. In the healthy subject at rest, the contribution of the RV to right heart systolic function is surpassed by the contribution of both left ventricular contraction and the respiratory pump. RV systolic function plays a contributory role during exercise and in patients with pulmonary hypertension. The RV compensates better for volume overload than for pressure overload and is more capable of sustaining chronic increases in load than acute ones. An impaired RV-pulmonary artery coupling leads to a major mismatch between RV function and arterial load ("afterload mismatch") and is associated progressively with a low cardiac output and a high RAP. Right ventricular dysfunction is involved in the pathophysiology of both cardiovascular and pulmonary diseases, and may partly explain the deleterious haemodynamic consequences of mechanical ventilation.

Early changes in myocardial perfusion patterns after myocardial infarction: relation with contractile reserve and functional recovery.

OBJECTIVES: The purpose of this study was to assess early temporal changes in myocardial perfusion pattern by myocardial contrast echocardiography (MCE) and their relation to myocardial viability in patients with reperfused acute myocardial infarction (AMI). BACKGROUND: Myocardial contrast echocardiography no-reflow is associated with poor contractile recovery after AMI. However, little is known regarding early reversibility of microvascular dysfunction and its relation to myocardial viability. METHODS: Intracoronary MCE was performed immediately after reflow and 9 days later in 28 patients with a first AMI and successful coronary recanalization (Thrombolysis in Myocardial Infarction trial grade 3 flow). Semiquantitative contrast score and wall motion score (WMS) were assessed in each initially asynergic segment at initial and repeat MCE study. Low dose dobutamine echocardiography (DE) was performed at day 10, and follow-up (FU) rest echocardiography was performed 6 weeks later. RESULTS: Among 200 initially asynergic segments, 49% exhibited no or heterogeneous contrast enhancement at initial MCE versus 24% at restudy (p < 0.001). Three groups of segments were defined according to early changes in contrast pattern: group A, "sustained no-reflow" (n = 17); group B, improved contrast score (n = 68), and group C, "sustained reflow" (n = 112). Group A segments showed no improvement in WMS at FU. In contrast, group B segments showed significant improvement in WMS at FU (p < 0.0001), and exhibited more frequently contractile reserve at DE (36% vs. 6%, p = 0.02) and contractile recovery at FU (34% vs. 7%, p = 0.03) than group A segments. Group C segments exhibited contractile reserve and contractile recovery in 47% and 51% of segments respectively. CONCLUSIONS: Improvement in MCE perfusion pattern may occur after initial no-reflow in the days following reperfused AMI and is associated with preservation of contractile reserve and gradual regional functional recovery.

Compensated cardiac hypertrophy: arrhythmogenicity and the new myocardial phenotype. I. Fibrosis.

The high incidence of arrhythmias in compensated cardiac hypertrophy is related to two independently regulated components-fibrosis and the adaptational phenotypic changes in membrane proteins linked to cardiac hypertrophy, and fibrosis. During the regression of hypertensive cardiopathy in middle-aged spontaneously hypertensive rats, the roles of cardiac hypertrophy and fibrosis can be analysed separately, revealing that both correlate independently with arrhythmias. In an experimental model of myocardial infarction it is possible to prevent arrhythmias with propranolol at the same time as cardiac hypertrophy, despite ventricular fibrosis. Fibrosis would appear to create arrhythmias both by anatomical uncoupling and by a re-entry mechanism generated by the zig-zag propagation of the transverse waveform. Triggered activity and automaticity depend on the membrane phenotype of the cardiocyte. They also play an important role, which is aggravated by myocardial heterogeneity.

Effects of sustained low-flow ischemia on myocardial function and calcium-regulating proteins in adult and senescent rat hearts.

OBJECTIVE: Both aging and myocardial ischemia are associated with alterations of calcium-regulating proteins. We investigated the effects of graded levels of low-flow ischemia on myocardial function and on SR Ca(2+)-ATPase (SERCA2), Na(+)-Ca2+ exchanger (NCX) and ryanodine receptor (RyR2), at mRNA and protein levels in both adult and senescent myocardium. METHODS: Isolated hearts from 4 and 24 month old (mo) rats were retrogradely perfused during 180 min at 100% (100% CF, n = 11 and n = 11 respectively. 30% (30% CF, n = 10 and n = 12) or 15% (15% CF, n = 13 and n = 8) of their initial coronary flow, and active tension and coronary resistance (in % of their baseline value) were recorded. After 180 min of perfusion. NCX, RyR2 and SERCA2 mRNAs (in % of age-matched 100% CF group value) and protein levels were quantitated in the left ventricles by slot blot and Western blot analysis, respectively. RESULTS: In 24 mo hearts, low-flow ischemia induced a greater fall in active tension (-65 +/- 7% vs. -40 +/- 4% in 4 mo 30% CF, p, 0.01 and -82 +/- 2% vs. -60 +/- 5% in 4 mo 15% CF groups, p < 0.05 after 15 min of ischemia) and a greater increase in coronary resistance (+357 +/- 44% vs. +196 +/- 39% in 4 mo 30% CF, p < 0.05 and +807 +/- 158% vs. +292 +/- 61% in 4 mo 15% CF groups, p < 0.001 after 15 min of ischemia). An increased accumulation of SERCA2 (+36% and NCX (+46%) transcripts, but not RyR2, already occurred in 24 mo 30% CF group while the 3 transcripts accumulated in 24 mo 15% CF group. In 4 mo rats SERCA2 (+26%), NCX (+35%) and RyR2 (+81%) mRNA levels only increased in the 15% CF group. Corresponding calcium-regulating protein levels were unaltered whatever the degree of flow reduction in both 4 mo and 24 mo hearts. CONCLUSION: Low-flow ischemia does not induce calcium-regulating protein loss in both adult and senescent hearts. The increase in mRNAs coding for calcium-handling proteins and the impairment of myocardial function which occur at a lesser degree of coronary flow reduction in senescent hearts, indicate a higher vulnerability to low-flow ischemia during aging.

Senescent heart compared with pressure overload-induced hypertrophy.

Although systolic left ventricular (LV) function is normal in the elderly, aging is associated in rat papillary muscle with mechanical and sarcoplasmic reticulum Ca2+ ATPase alterations similar to those observed in the hypertrophied heart. However, alterations in the other calcium-regulating proteins implicated in contraction and relaxation are still unknown. To investigate alterations in LV function and calcium-regulating proteins, we measured hemodynamics and Na(+)-Ca2+ exchanger (NCx), ryanodine receptor (RyR2), and sarcoplasmic reticular Ca2+ ATPase (SERCA2) mRNA levels (expressed in densitometric scores normalized to that of poly(A+) mRNA) in left ventricle from 4-month-old (adult, n = 13) and 24-month-old (senescent, n = 15) rats. For ex vivo contractile function, active tension was measured during isolated heart perfusion in adult (n = 11) and senescent (n = 11) rats. For comparison of age-dependent effects of moderate hypertension on both hemodynamics and calcium proteins, renovascular hypertension was induced or a sham operation performed at 2 (n = 11 and n = 6) and 22 (n = 26 and n = 5) months of age. In senescent rats, LV systolic pressure and maximal rates of pressure development were unaltered, although active tension was depressed (4.7 +/- 0.4 versus 8.3 +/- 0.7 g/g heart weight in adults, P < .0001). SERCA2 mRNA levels were decreased in senescent left ventricle (0.98 +/- 0.05 versus 1.18 +/- 0.05 in adults, P < .01), without changes in NCx and RyR2 mRNA accumulation. Renovascular hypertension resulted in 100% mortality in aged rats; in adults, renovascular hypertension resulted, 2 months later, in an increase of LV systolic pressure (170 +/- 7 versus 145 +/- 3 mm Hg in sham-operated rats, P < .05) and in mild LV hypertrophy (+18%, P < .01) associated with a decrease in SERCA2 mRNA levels (1.02 +/- 0.03 versus 1.18 +/- 0.03 in sham-operated rats, P < .001). Contractile dysfunction in senescent isolated heart and decreased SERCA2 mRNA levels were associated with in vivo normal LV function at rest, indicating the existence of in vivo compensatory mechanisms. RyR2 and NCx gene expressions were not implicated in the observed contractile dysfunction. In aged rats, renovascular hypertension resulted in 100% mortality, probably related to elevated levels of circulating angiotensin II, whereas in adult rats, renovascular hypertension induced a mild LV hypertrophy associated with a selective alteration in SERCA2 gene expression.

Utility of indium-111-antimyosin scintigraphy for diagnosis of myocardial damage in systemic sclerosis.

The diagnosis of myocardial disease related to systemic sclerosis is often difficult, but it is clinically relevant since the occurrence of a specific ventricular dysfunction is of poor prognosis. This article reports a case of systemic sclerosis with a subacute episode of myocardial disease assessed by 111In-antimyosin antibody, a specific marker of the necrotic myocardial fiber.

Relationship between resting 201Tl reverse redistribution, microvascular perfusion, and functional recovery in acute myocardial infarction.

UNLABELLED: 201TI reverse redistribution is a common finding early after reperfusion therapy for myocardial infarction. Its mechanism and clinical implications remain unclear. The aim of this study was to clarify the relationships between reverse redistribution, microvascular perfusion, and myocardial viability. METHODS: Resting, 10-min-postinjection, and redistribution 201TI data obtained for 33 patients 8 and 42 d after the onset of acute myocardial infarction were compared with echocardiographic wall motion measured acutely and on day 42. Microvascular perfusion was assessed by myocardial contrast echocardiography performed 10 min after restoration of complete patency of the infarct artery. RESULTS: Marked significant reverse redistribution was found on day 8 (absolute change, 7.5%+/-7.9% of the 10-min-postinjection defect size; P<5x0.000001) and significantly decreased on day 42 (2.7%+/-6.8%; P = 0.004 between days 8 and 42). The 10-min-postinjection defect size best predicted the final infarct size on day 42 and was closely related to microvascular perfusion. Patients with adequate reperfusion had a smaller postinjection defect on day 8 (21.1%+/-14.6%) and a larger reverse redistribution (10.2%+/-6.1%) than did patients with no reflow (35.3%+/-13% and 3.2%+/-9.2%, respectively; P<0.04 for both). CONCLUSION: Reverse redistribution was marked early after myocardial infarction in patients with complete patency of the infarct artery and decreased in subsequent weeks. Reverse redistribution was associated with restoration of adequate microvascular reperfusion and with myocardial salvage and viability. The early postinjection scans on day 8 were the relevant images for assessing myocardial salvage and predicting wall motion recovery.

European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias.

Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)

Alteration of the alveolar-capillary membrane diffusing capacity in chronic left heart disease.

During left heart disease, the chronic increase in pulmonary capillary wedge pressure (PCWP) results both in vascular alterations with increased pulmonary vascular resistance (PVR), and in progressive thickening of the alveolar-capillary membrane, which diffusing capacity (Dm) is reduced. However, the total lung diffusing capacity for carbon monoxide (TLco) is inconstantly impaired, depending on the degree of pulmonary congestion. We evaluated the relation between the pulmonary hemodynamic repercussions of chronic heart disease and the 2 components of TLco, i.e., Dm and capillary blood volume. Forty-seven patients with chronic left heart disease (28 with valve disease, 19 with cardiomyopathy) underwent right heart catheterization with determination of PCWP and PVR. Pulmonary function tests, including spirometry, determination of TLco, and of its 2 components (percentage of predicted values) were performed in patients and in 15 healthy subjects. TLco and Dm, but not capillary blood volume, were significantly decreased in patients. Dm was related to PVR (p = 0.0006), and was markedly reduced in patients with high PVR (> or = 3 Wood U): 54 +/- 8% vs 80 +/- 19% in patients with normal PVR (p <0.0001). Dm < or = 66% identified all high PVR patients (sensitivity = 100%, specificity = 77%). Capillary blood volume was related to PCWP (p = 0.02), and was increased in patients with high PCWP (> 15 mm Hg): 126 +/- 30% vs 99 +/- 23% (p <0.01), but with a marked overlap. TLco values, although reduced in patients with high PVR (p <0.001), were not predictive of high PVR or high PCWP. Determination of Dm allows a more accurate detection of pulmonary hypertension complicating chronic left heart disease than the other pulmonary parameters.

Molecular and cellular biology of the senescent hypertrophied and failing heart.

During aging, experimental studies have revealed various cellular changes, principal among which is myocyte hypertrophy, which compensates for the loss of myocytes and is associated with fibrosis. The expression of alpha-myosin heavy chain is replaced by that of the isogene beta-myosin, which leads to decreased myosin adenosine triphosphatase (ATPase) activity. In consequence, contraction is slower and more energetically economical. The Ca(2+)-ATPase of the sarcoplasmic reticulum and Na+/Ca2+ exchange activity are decreased, which probably explains the reduced velocity of relaxation. Membrane receptors are also modified, since the density of both the total beta-adrenergic and muscarinic receptors is decreased. The senescent heart is able to hypertrophy in response to overload and to adapt to the new requirements. Similar alterations are observed both in the senescent heart and in the overloaded heart, in clinical as well as in experimental studies; however, differences do exist, especially in terms of fibrosis and arrhythmias.

Nonlimited exercise test combined with high-dose dipyridamole for thallium-201 myocardial single-photon emission computed tomography in coronary artery disease.

Clinical, electrocardiographic, and thallium-201 single-photon emission computed tomography data were evaluated in 397 consecutive patients divided into 3 groups according to coronary hyperemic stimulation: 186 patients (group I; Ex) had maximal symptom-limited exercise ergometric stress testing, 93 patients (group II; Dip) had intravenous dipyridamole (0.7 to 0.8 mg/kg) stress testing, and 118 patients (group III; Dip+Ex) had dipyridamole (0.7 to 0.8 mg/kg) plus nonlimited (i.e., symptom-limited) exercise stress testing, achieving a maximal workload (mean +/- SD) of 102 +/- 37 W. Clinical tolerance was higher in Ex than in Dip groups (p < 0.01), and tended to be higher in Dip+Ex than in Dip groups (p = NS). Image quality--as judged by signal-to-noise ratios--was superior in Ex and Dip+Ex groups when compared with the Dip group (p < 0.01). Chest pain and electrocardiographic positivity were more frequent in the Dip+Ex group than in the Dip group (p < 0.05), despite more extensive coronary artery disease (CAD) in the Dip group; and reversible scintigraphic defects were more frequent in Dip+Ex versus Dip (p < 0.01) and in Ex versus Dip groups (p < 0.05) in patients with established CAD, as well as for the whole group. We conclude that, in patients unable to achieve 85% of their maximal predicted heart rate, the combination of high-dose dipyridamole plus nonlimited exercise stress testing is superior to dipyridamole stress testing alone, and comparable to maximal exercise testing.

Comparison of the prognostic value of C-reactive protein and troponin I in patients with unstable angina pectoris.

This study assessed the prognostic value of cardiac troponin I (cTnI) and C-reactive protein (CRP) in unstable angina, and specifically in patients with angiographically proven coronary artery disease. These biochemical parameters, which are related to myocardial injury or to systemic inflammation, may help in short-term risk stratification of unstable angina. We prospectively studied 195 patients with unstable angina, 100 of whom had angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/ml) and CRP (N < 3 mg/L) were measured at admission, 12, and 24 hours later. The rate of in-hospital major adverse cardiac events (death, myocardial infarction, or emergency revascularization) was higher in patients with increased cTnI within the first 24 hours, regardless of the results of coronary angiography (23% vs 7%; p < 0.001). Conversely, events occurred at similar rates in patients with or without increased CRP. In patients with angiographic evidence of coronary artery disease, multivariate analysis showed that increased cTnI within 24 hours of admission (35 patients) was an independent predictor of major adverse cardiac events (odds ratio 6.7, range 1.7 to 27.3), but not cTnI levels at admission and CRP at 0, 12, and 24 hours. Thus, both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome. We also found a temporal link between cTnI increase and late elevation of CRP, suggesting that systemic inflammation may partially be a consequence of myocardial injury.

The O'Brien-Angell stentless porcine valve: early results with 150 implants.

From August 1991 to June 1994, 150 patients underwent aortic valve replacement with the O'Brien-Angell stentless porcine xenograft (Bravo Cardiovascular Model 300, Cryolife, Atlanta, GA). To establish trends we analyzed three consecutive groups of 50 patients. We found significant differences in low postoperative gradients (mean < or = 10 mm Hg): 24% in group 1, 42% in group 2, and 96% in group 3. Comparing groups 1 and 3, gradients were significantly lower in all valve sizes. The difference is credited to better supraannular positioning of the valve, which is the key to the learning curve. Trivial central regurgitation was present in the three groups at 6%, 12%, and 0%, respectively. Peripheral regurgitation was trivial in 6%, 8%, and 0%, and mild to moderate in 4%, 2% and 0%, respectively. Seventy-eight of 107 patients with an available follow-up exceeding 1 year had noninvasive controls. Two early cases with moderate perivalvular leaks evolved to moderately severe leaks. Two valves were explanted. The O'Brien-Angell stentless valve is easy to handle and correct supraannular positioning provides excellent hemodynamic results.

Molecular characteristics of cocaine-induced cardiomyopathy in rats.

Cocaine abuse induces severe cardiomyopathy. To investigate the molecular effects of acute and prolonged administration of cocaine, mRNAs encoding markers of either mechanical overload, as atrial natriuretic factor (ANF) and alpha- and beta-myosin heavy chains, or fibrosis as type I and III procollagens, were quantitated in the left ventricle of rats 4 h after one injection of cocaine (40 mg/kg, n = 7), or 14 (n = 15) and 28 days (n = 10) after chronic infusion of cocaine (40 mg/kg per day). Plasma cocaine and benzylecgonine concentrations were both significantly augmented during the infusion while plasma levels of triiodothyronine and thyroxine were lowered. Acute injection of cocaine induced ANF gene expression. Cocaine treatment during 28 days resulted in left ventricular hypertrophy (+ 20% after 24 days, P < 0.05) with normal blood pressure, associated with an accumulation of mRNAs encoding ANF and type I and III collagens (+66% and +55%, P < 0.05). Such a chronic treatment also induced a shift from the alpha- to the beta-myosin heavy chain gene expression (-40% and +50%, P < 0.05). In conclusion, cocaine activates markers of both hemodynamic overload and fibrosis. Such an activation may result from direct and/or indirect effects of the drug such as myocardial ischemia, mechanical overload and/or hypothyroidism.

Acute assessment of microvascular perfusion patterns by myocardial contrast echocardiography during myocardial infarction: relation to timing and extent of functional recovery.

OBJECTIVE: To examine the relation between the initial microvascular perfusion pattern, as assessed by intracoronary myocardial contrast echocardiography (MCE), immediately after restoration of TIMI (thrombolysis in myocardial infarction) (TIMI) grade 3 flow during acute myocardial infarction, and the extent and timing of functional recovery in the area at risk. SETTING: Referral centre for interventional cardiology. METHODS: Intracoronary MCE was performed 15 minutes after TIMI grade 3 recanalisation of the infarct artery in 25 patients. Segmental myocardial contrast patterns were graded semiquantitatively (0, none; 0.5, heterogeneous; 1, homogeneous). Functional recovery was assessed by echocardiography on days 9 and 42. RESULTS: Among 174 myocardial segments in the area at risk, wall motion recovery on day 9 was observed in 40% of MCE grade 1 segments but there was no significant recovery in grade 0 or 0.5 segments. On day 42, recovery had occurred in 56% of MCE grade 1 segments (p < 0. 0001 v MCE grade 0 and 0.5; p = 0.0001 v MCE grade 1 on day 9), and 22% of MCE grade 0.5 segments (p = 0.02 v MCE grade 0; p = 0.0005 v MCE grade 0.5 on day 9); MCE grade 0 segments did not recover. Negative predictive value in predicting recovery by contrast enhancement was 95% and 89% by days 9 and 42, respectively. CONCLUSIONS: Contractile recovery occurs earliest in well reperfused segments. Up to one quarter of segments with heterogeneous contrast enhancement show wall motion recovery within the first six weeks. Myocardial perfusion after recanalisation in acute myocardial infarction, even if heterogeneous, is a prerequisite for postischaemic functional recovery. Thus preservation of acute myocardial perfusion is associated with more complete and early functional recovery.

Pulmonary time-of-flight MR angiography at 1.0 T: comparison between 2D and 3D tone acquisitions.

The purpose of this study was to compare the performance of 2D vs. 3D time-of-flight (TOF) methods in imaging the normal pulmonary arteries with commercially available 1.0 T equipment. The study was conducted in 20 volunteers and 7 patients with suspected pulmonary embolism (PE). To reduce artifacts caused by cardiac and respiratory motion, MR images were acquired in volunteers using two-dimensional (2D), gradient-recalled echo (GRE), breath-hold techniques, and three-dimensional (3D) acquisitions. Sagittal thin (6-MM) segmented k-space 2D sections obtained with cardiac gating during systole (turboFLASH, TR/TE9/6 ms, 14 segments of 9 lines) and incremented flip-angles (TONE), and 50-mm 3D volume TONE acquisitions with 32 partitions (FISP, TR/TE34/10ms) were successively performed. In the second phase of the study, patients were examined only with the 3D technique. Images of volunteers were qualitatively and quantitatively analyzed. S/N ratios were statistically compared by means of the paired-sample Wilcoxon ranked-signed test, a value of p < .05 being significant. In volunteers, 3D acquisitions displayed significantly more segment-order pulmonary arteries on average than did 2d acquisitions displayed significantly more segment-order pulmonary arteries on average than did 2D acquisitions (2.95 +/- 0.64 vs. 2.2 +/- 0.85, respectively; p < .01). Moreover, the signal intensity of arteries within the lungs was less homogeneous in the 2D than in the 3D technique, with a signal intensity ratio between peripheral and proximal arteries of 63% +/- 7% and 73% +/- 2%, respectively (p < .05). In patients, no erroneous diagnoses were obtained using the 3D technique. 3D images of normal lungs provide MR angiograms of better quality than do 2D images, and require less contribution from subjects because they are performed in free breathing. Ongoing improvements in MR sequences and further studies are now necessary to assess the value of 3D TONE MRA in the diagnosis of PE.

Early isonitrile SPECT in acute myocardial infarction: feasibility and results before and after fibrinolysis.

Early 99Tcm-labelled methoxy-isobutyl-isonitrile (MIBI) SPECT was performed in 14 patients with suspected acute myocardial infarction (AMI). The radiopharmaceutical was administered immediately upon admission to the intensive care unit and before any diagnostic confirmation. Then, if decided, thrombolytic therapy was started. Cardiac imaging was performed 1 h later, and as there is no significant re-distribution, the pictures still showed the pre-treatment MIBI uptake. In three cases acute myocardial infarction was not confirmed. For one of them, the result was normal and this patient was ultimately considered to have had a transient ischaemic event. The two other cases had acute chest pain with a previous history of myocardial infarction (MI) and a pathological MIBI SPECT. In the 11 cases with confirmed first AMI significant perfusion defect was seen. For every patient a new MIBI injection with a control SPECT was repeated 72 h after admission. Eight patients were seen 1 h 15 min to 3 h 15 min after the onset of chest pain and had thrombolytic therapy. Defects were always in agreement with coronary angiography and 2D echocardiography performed in the same period. After thrombolysis, control SPECT showed no recovery in three cases, partial recovery in four, and nearly complete recovery in one. Using this technique, it was then possible to get high quality myocardial perfusion imaging without delaying treatment of AMI. This preliminary series suggests that MIBI SPECT may be useful in accurately showing the size and location of the immediate perfusion defect, and in assessing the response to emergency therapy of AMI, especially thrombolysis.

NC100100, a new echo contrast agent for the assessment of myocardial perfusion--safety and comparison with technetium-99m sestamibi single-photon emission computed tomography in a randomized multicenter study.

BACKGROUND AND HYPOTHESIS: Myocardial contrast echocardiography using second-generation agents has been proposed to study myocardial perfusion. A placebo-controlled, multicenter trial was conducted to evaluate the safety, optimal dose, and imaging mode for NC100100, a novel intravenous second-generation echo contrast agent, and to compare this technique with technetium-99m sestamibi (MIBI) single-photon emission computed tomography (SPECT). METHODS: In a placebo-controlled, multicenter trial, 203 patients with myocardial infarction > 5 days and < 1 year previously underwent rest SPECT and MCE. Fundamental and harmonic imaging modes combined with continuous and electrocardiogram-- (ECG) triggered intermittent imaging were used. Six dose groups (0.030, 0.100, and 0.300 microliter particles/kg body weight for fundamental imaging; and 0.006, 0.030, and 0.150 microliter particles/kg body weight for harmonic imaging) were tested. A saline group was also included. Safety was followed for 72 h after contrast injection. Myocardial perfusion by MCE was compared with myocardial rest perfusion imaging using MIBI as a tracer. RESULTS: NC100100 was well tolerated. No serious adverse events or deaths occurred. No clinically relevant changes in vital signs, laboratory parameters, and ECG recordings were noted. There was no significant difference between adverse events in the NC100100 (25.7%) and in the placebo group (17.9%, p = 0.3). Intermittent harmonic imaging using the intermediate dose was superior to all other modalities, allowing the assessment of perfusion in 76% of all segments. Eighty segments (96%) with normal perfusion by SPECT imaging also showed myocardial perfusion with MCE. However, a substantial percentage of segments (61-80%) with perfusion defects by SPECT imaging also showed opacification by MCE. This resulted in an overall agreement of 66-81% and a high specificity (80-96%), but in low sensitivity (20-39%) of MCE for the detection of perfusion defects. CONCLUSION: NC100100 is safe in patients with myocardial infarction. Intermittent harmonic imaging with a dose of 0.03 microliter particles/kg body weight can be proposed as the best imaging protocol. Myocardial contrast echocardiography with NC 100100 provides perfusion information in approximately 76% of segments and results in myocardial opacification in the vast majority of segments with normal perfusion as assessed by SPECT. Although the discrepancies between MCE and SPECT with regard to the definition of perfusion defects requires further investigation, MCE with NC 100100 is a promising technique for the noninvasive assessment of myocardial perfusion.

[Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases]. / Effet anti-arythmique de la propafénone per os. A propos de 70 observations.

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.