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P Assayag

Publications and source records attributed to P Assayag.

At least 19 recordsLinked to original sources

Serial evaluation of perfusion defects in patients with a first acute myocardial infarction referred for primary PTCA using intravenous myocardial contrast echocardiography.

AIMS: To investigate whether myocardial contrast echocardiography using Sonazoid could be used for the serial evaluation of the presence and extent of myocardial perfusion defects in patients with a first acute myocardial infarction treated with primary PTCA, and specifically, (1) to evaluate safety and efficacy of myocardial contrast echocardiography to detect TIMI flow grade 0--2, (2) to evaluate the success of reperfusion and (3) to predict left ventricular recovery after 4 weeks follow-up. METHODS AND RESULTS: Fifty-nine patients underwent serial myocardial contrast echocardiography, immediately before primary PTCA (MCE1), 1 h (MCE2) and 12--24 h after PTCA (MCE3). A perfusion defect was observed in 21 of 24 patients (88%) with anterior acute myocardial infarction. All but one had TIMI flow grade 0--2 prior to PTCA. Nine of 31 patients (29%) with inferior acute myocardial infarction showed a perfusion defect and all had TIMI flow grade 0-2 prior to PTCA. Restoration of TIMI flow grade 3 was achieved in 73% of the patients by primary PTCA. A reduction in size of the initial perfusion defect of at least one segment (16 segment model) or no defect vs persistent defect in patients with anterior acute myocardial infarction was associated with improved global left ventricular function at 4 weeks; mean global wall motion score index 1.29+/-0.21 vs 1.66+/-0.31 (P=0.009). Multiple regression analysis in patients with an anterior acute myocardial infarction revealed that the extent of the perfusion defect at MCE3 was a significant (P=0.0005) independent predictor for left ventricular recovery at 4 weeks follow-up. The only other independent predictor was TIMI flow grade 3 post PTCA (P=0.007). CONCLUSION: Intravenous myocardial contrast echocardiography immediately prior to primary PTCA seems safe and is capable of detecting the presence of a perfusion defect and its subsequent dynamic changes, particularly in patients with a first anterior acute myocardial infarction. A significant reduction in size of the initial perfusion defect using serial myocardial contrast echocardiography predicts functional recovery after 4 weeks and these findings underscore the potential diagnostic value of intravenous myocardial contrast echocardiography.

Aged↗

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.

Coronary Circulation↗

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.

Aged↗

Elevated cardiac troponin I predicts a high-risk angiographic anatomy of the culprit lesion in unstable angina.

BACKGROUND: This study assessed the relation between the angiographic appearance of the culprit lesion and cardiac troponin I (cTnI) or C-reactive protein (CRP) elevations within the first 24 hours in unstable angina. Intracoronary thrombus or a complex morphology, is frequently observed on angiography in patients with unstable angina and is associated with a higher rate of spontaneous or coronary angioplasty-related complications. Biochemical parameters related to myocardial injury (eg, cTnI) or to systemic inflammation (eg, CRP) are known prognostic markers for clinical outcome and may help in angiographic risk stratification to provide new adjunctive therapy. METHODS AND RESULTS: We studied 100 patients admitted for unstable angina with 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 and 12 and 24 hours later. Multivariate analysis showed that elevated cTnI (>/=0.4 ng/mL) within 24 hours (35 patients) was an independent predictor of an angiographic appearance of the culprit lesion carrying a high risk of major cardiac events in the outcome and whether angioplasty is attempted (coronary thrombus, occlusion, or type C lesions; odds ratio 4.1, 1. 6 to 10.5). cTnI levels at admission and CRP at 0, 12, and 24 hours were not predictive of high-risk angiographic anatomy. CONCLUSIONS: In patients with unstable angina and angiographically proven coronary artery disease, increased cTnI within 24 hours of admission but not increased CRP is associated with an angiographic appearance of the culprit lesion carrying a high risk of complication, especially in the event of angioplasty.

Angina, Unstable↗

Decreased no-reflow in patients with anterior myocardial infarction and pre-infarction angina.

AIMS: Pre-infarction angina is associated with better outcome after myocardial infarction. The aim of this study was to assess whether pre-infarction angina is associated with decreased no-reflow after coronary recanalization. METHODS AND RESULTS: Twenty-three patients underwent intracoronary myocardial contrast echocardiography during the acute phase of anterior myocardial infarction after successful recanalization, and before hospital discharge. Myocardial perfusion was graded semi-quantitatively in the area at risk (dyssynergic segments). Global left ventricular function was assessed by radionuclide angiography on days 8 and 42 and regional wall motion was assessed by 2D echocardiography on days 0 and 42. Fourteen patients had pre-infarction angina (angina less than 7 days before myocardial infarction) and nine did not. Baseline characteristics were similar in the two groups. The myocardial contrast echocardiography perfusion score in the area at risk after recanalization was higher in the patients with pre-infarction angina than in those without (0.72 +/- 0.19 vs 0.53 +/- 0.22, P=0.04), and the incidence of no-reflow (myocardial contrast echocardiography perfusion score < or =0.5) was lower (14% vs 56%, P=0.04). This difference persisted 8 +/- 2 days after myocardial infarction (0. 87 +/- 0.11 vs 0.69 +/- 0.26, P=0.04), and was associated with greater mid-term (day 42) improvement in left ventricular function in patients with pre-infarction angina than in those without, as assessed by changes in radionuclide left ventricular ejection fraction (+5.8 +/- 8.1% vs -3.3 +/- 4.6%, respectively;P=0.01) and by changes in regional wall motion score on 2D echocardiography (-0. 61 +/- 0.39 vs -0.24 +/- 0.17, respectively;P=0.04). CONCLUSION: Pre-infarction angina is associated with preservation of the microvasculature, reflected by reduced no-reflow. This may be a mechanism underlying greater recovery of left ventricular function in patients with pre-infarction angina.

Adult↗

Partial rupture of the tricuspid valve after extraction of permanent pacemaker leads: detection by transesophageal echocardiography.

Traumatic lesions of the tricuspid valve complicating pacemaker lead extractions appear to be rare. We report two cases of partial rupture of the tricuspid valve, following apparently uneventful extraction of permanent ventricular leads, resulting in severe regurgitation and, in one case, chronic heart failure. TEE was useful to identify the traumatic mechanism of tricuspid regurgitation (TR) and the extent of valvular lesions in these patients. Such etiology should be suspected, and TEE performed, in patients developing TR or heart failure late after lead extraction.

Aged↗

111Indium antimyosin antibody imaging of primary myocardial involvement in systemic diseases.

OBJECTIVE: The diagnosis of primary myocardial involvement in systemic diseases is clinically relevant but difficult in the absence of specific criteria. Whatever the underlying disease, myocytes degeneration is observed during the active phase of myocardial damage. The aim of this study was to assess the diagnostic value of scintigraphic imaging with 111Indium antimyosin antibody (AM), a specific marker of the damaged myocyte, for ongoing myocardial damage related to systemic diseases. METHODS: 40 patients with histologically confirmed systemic diseases were studied. They were classified into two groups according to the presence (group 1, n = 30), or the absence (group 2, n = 10) of clinical, electrocardiographic (ECG) or echocardiographic signs suggestive of myocardial involvement. Planar and tomographic acquisitions were obtained 48 hours after injection of AM (90 MBq). Rest 201thallium (T1) scintigraphy was also performed to assess myocardial perfusion and scarring. Clinical, ECG, and echocardiographic +/- scintigraphic evaluations were repeated during follow up (17 +/- 19 months) in 36 of 40 patients. RESULTS: In group 1, 13 of 30 patients (43%) showed diffuse significant AM uptake throughout the left ventricle (LV), and no or mild T1 abnormality. Two of these were asymptomatic, four had normal ECG, and two had no clinical or echographic LV dysfunction. All patients in group 2 had negative AMA scintigraphy and normal T1 scintigraphy. During follow up of 12 AM positive patients, cardiac status improved after immunosuppressive treatment was intensified in nine cases, worsened in two cases, and remained stable in one. During follow up of 24 AM negative patients, cardiac status remained stable in 23 cases despite treatment not being increased in 20, including two patients with sequellary myocardial involvement. The last patient developed mild LV dysfunction after 36 months. CONCLUSION: AM scintigraphy allows detection of active myocardial damage related to systemic diseases, with increased specificity compared with conventional methods, and increased sensitivity in some cases. Further studies are needed to assess the potential value of AM scintigraphy as a therapeutic guide.

Adult↗

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.

Adult↗

[Applications of contrast echocardiography in the acute phase of myocardial infarction].

The present interest in myocardial contrast echocardiography is related to the development of new contrast agents which can be used intravenously and the perfection of new echocardiographic technologies. Amongst the potential applications of this technique, the study of myocardial perfusion in the acute phase of myocardial infarction is one of the most promising as shown by the experience acquired over several years with intracoronary contrast echocardiography. It allows assessment of the extent of the zones at risk before recanalisation, the presence of collateral vessels and, above all, the quality of myocardial reperfusion. The demonstration of the absence of effective reperfusion of the myocardial microcirculation, or the phenomenon of no-reflow, is one of the main advantages of contrast echocardiography and has been identified as an important independent prognostic factor. This technique could therefore become essential in the evaluation of methods for reducing the extent of microvascular damage. Although many questions remain unanswered about the ideal methods of performing and analysing intravenous contrast echocardiography, the preliminary results confirm the potential of the technique in non-invasive evaluation of myocardial reperfusion in the acute phase of myocardial infarction.

Contrast Media↗

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.

Angina, Unstable↗

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.

Adult↗

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.

Aging↗

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.

Adult↗

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.

Animals↗

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.

Animals↗

The stentless Bravo 300 aortic porcine xenograft: supra-annular versus annular implantation.

The aim of the study was to compare the supra-annular and intra-annular implantation techniques by evaluating the differences in early haemodynamic outcome (gradients, effective orifice area, regurgitation). Since August 1991, 200 stentless Bravo model 300 valves have been implanted. Patients were divided into three groups of consecutive cases: group 1 (n = 50) represents exclusively intra-annular implantation; group 2 (n = 50) is a transitional period: and group 3 (n = 100) comprises only patients with supra-annular implantation. Significant differences were found (P<0.001) in low postoperative gradients (mean < or = 10 mmHg): 24% in group 1, 42% in group 2, and 95% in group 3. Comparing groups 1 and 3, gradients were lower and effective orifice area was augmented in all valve sizes in group 3. Trivial central regurgitation was present in groups 1-3 (6%, 12% and 0% respectively). Peripheral regurgitation was trivial in 6%, 8% and 0% and mild to moderate in 4%, 2% and 0% (P<0.001).

Animals↗

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.

Aging↗