Cristina Piccinino

Dipyridamole echocardiography test. A new tool for detecting jeopardized myocardium after thrombolytic therapy.

BackgroundWe wished to assess whether dipyridamole echocardiography test (DET) can detect jeopardized myocardium after thrombolytic therapy. Methods and ResultsSeventy-six consecutive patients with a first acute myocardial infarction (AMI) were treated with 2 million IU urokinase i.v. within 4 hours of the onset of AMI and underwent high-dose (as much as 0.84 mg/kg over 10 minutes) DET 8–10 days after AMI. The results were correlated to the anatomy of the infarct-related vessel (IRV). In patients with positive DET, we evaluated the wall motion score index (WMSI; a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of interpreted segments. In a 13-segment model, each segment was assigned a score ranging from 1 (normal) to 4 (dyskinetic). Fifty-three patients had positive results on DET. Of these, 42 had dipyridamoleinduced new wall motion abnormalities (WMAs) confined to the infarct zone or adjacent segments. In these patients, mean WMSI increased from 1.46 ± 0.26 (at resting conditions) to 1.73 ± 0.35 (at peak dipyridamole) (p < 0.01), whereas no significant change was detected in negative patients (1.6 ± 0.34 versus 1.57 ± 0.34, p = NS). Coronary angiography showed a patent IRV (TIMI grade 2 or 3) in 53 patients and no or minimal reperfusion (TIMI grade 0 or 1) in 23 patients. A patent IRV with critical residual stenosis was found in 35 of 42 patients with dipyridamole-induced WMAs in the infarct zone and in 18 of 34 patients without WMAs (p < 0.05). Among the 23 patients with occluded IRVs, nine had collateral flow to the distal vessel; six of these had a positive DET. Thus, the sensitivity and specificity for identifying a critically stenotic but patent IRV or the presence of a collateral-dependent zone were 66% and 93%, respectively. In a subset of nine patients with a positive DET in the infarct zone or adjacent segments, DET and a control coronary angiography were repeated 1-3 months after an angiographically successful (residual stenosis, 50% or less) coronary angioplasty in the IRV. The repeat DET was negative in eight patients (all with patent IRV at control angiography) and again positive in one patient, who showed restenosis at angiography. The WMSI at resting conditions was similar before and after angioplasty, whereas it differed significantly at peak dipyridamole (1.7 ± 0.2 versus 1.4 ± 0.2, p < 0.01). ConclusionsDET can identify the anatomy of the IRV, and dipyridamole-induced WMAs within the infarct zone detect regions with jeopardized myocardium that may benefit from intervention.

Left atrial asynchrony is a major predictor of 1-year recurrence of atrial fibrillation after electrical cardioversion.

Background The level of atrial mechanical asynchrony may vary within the atrial fibrillation population and this may have pathophysiological relevance. Objective We sought to verify whether the degree of left-atrial mechanical asynchrony associated with atrial fibrillation is a predictor of arrhythmia recurrence after restoration of sinus rhythm with electrical cardioversion. Methods and results Left atrial volume was calculated, whereas two-dimensional (2D) strain (speckle tracking technique) was used to estimate peak and standard deviation (SD) of time-to-peak of deformation of six segments arbitrarily identified along the perimeter of the cavity, imaged in apical four-chamber view. Left atrial mechanical asynchrony was quantified according to quartiles of time-to-peak SD assuming that larger values would identify higher grades of asynchrony. A total of 130 patients undergoing cardioversion for atrial fibrillation were prospectively enrolled. Time-to-peak SD was inversely related with peak strain (P < 0.001). No differences were observed among groups in terms of clinical, therapeutical and additional echocardiographic variables. At 1-year atrial fibrillation was observed in 53% of patients, with time-to-peak SD linearly related to atrial-fibrillation recurrence (P = 0.014). At multivariate analysis only time-to-peak SD (P = 0.032), but not atrial volume (P = 0.075), was identified as an independent predictor of fibrillation recurrence. Conclusion This is the first study showing that left atrial asynchrony, quantified as time-to-peak SD of regional atrial strains before electrical cardioversion, is a major independent predictor of fibrillation recurrence in patients back to sinus-rhythm postprocedure.

Cardiac Dyssynchrony Quantitated by Time-to-Peak or Temporal Uniformity of Strain at Longitudinal, Circumferential, and Radial Level: Implications for Resynchronization Therapy

BACKGROUND The standard deviation of time to peak strain (TPS-SD) has been proposed as an index of left ventricular (LV) dyssynchrony in patients to be resynchronized. However, TPS-SD is sensitive to noise, and the influence of outliers on TPS-SD is also relevant. Alternatively, dyssynchrony can be indexed by temporal uniformity of strain (TUS), whereby a time plot of regional strains, arranged for LV location, is subjected to Fourier analysis. If segments shorten simultaneously (synchronously), the plot appears as a straight line, with power only in the zero-order Fourier term, whereas regionally clustered dyssynchrony generates an undulating plot with higher power in the first-order term. TUS index reflects zero-order relative to first-order plus zero-order power. METHODS In this study, TUS and TPS-SD were computed in 68 patients (QRS duration >/= 120 ms; ejection fraction </= 0.35) in whom longitudinal, circumferential, and radial strains were measured using speckle-tracking two-dimensional echocardiography before and 3 to 6 months after cardiac resynchronization therapy (CRT), together with LV volumes. RESULTS Following CRT, LV volume decreased (diastolic, -10 +/- 20%) and ejection fraction improved from 0.23 +/- 0.07% to 0.30 +/- 0.10% (P < .001 for both). Circumferential strain was ameliorated as well (P = .054). Two-way analysis of variance revealed TUS improvement after CRT (P = .043), with a trend for CRT to contrast asynchrony at the circumferential (+0.06 +/- 0.25) and longitudinal (+0.05 +/- 0.18) levels compared with the radial level (-0.002 +/- 0.18) (interaction P = .06). This was not true for TPS-SD. Multivariate analysis revealed that only TUS, assessed before CRT circumferentially, predicted ejection fraction improvement after CRT. Other asynchrony variables failed in the model. CONCLUSION Dyssynchrony indexed by circumferential TUS yields greater CRT benefits than that indexed by TPS-SD, supporting the idea of targeting TUS-measured dyssynchrony as a more informative quantitative measurement in CRT patients.

Lack of Influence of Atrioventricular Delay on Stroke Volume at Rest in Patients with Complete Atrioventricular Block and Dual Chamber Pacing

Dual chamber pacing (DDD) maintains atrioventricular (AV) sequence; AV delay program mobility modifies the relationship between atrial and ventricular contraction. To evaluate the hemodynamic effects of such a modification, ten patients with a DDD unit for complete AV block were studied by time‐motion (M‐mode) and Doppler echocardiography during inhibited ventricular pacing (VVI), atrial‐triggered ventricular pacing (VDDJ and atrioventricular sequential pacing (DVI) at different AV delay (90, 140, 390, 240 msec). A significant improvement in stroke volume (SV) (15%–20%, P < 0.05) was seen during DDD versus VVI pacing; no changes, however, were observed in the same patient with different AV delay or during DVI versus VDD pacing. These data suggest that programming of AV delay does not affect systolic performance at rest; longer diastolic filling times recorded during DDD pacing with “short” AV delay (90–340 msec) do not seem to be a hemodynamically relevant epiphenomenon of PM programming.

Early assessment of coronary artery bypass graft patency by high-dose dipyridamole echocardiography

Abstract To assess the role of high-dose (up to 0.84 mg/kg during 10 minutes) dipyridamole echocardiographic testing in the evaluation of coronary artery bypass graft patency early after surgery, 18 consecutive patients with angina underwent dipyridamole echocardiography and coronary angiography before and 7 to 10 days after bypass surgery-Coronary angiography showed 2- or 3-vessel disease in 7 and 11 patients, respectively. A total of 53 bypass grafts were performed. Before bypass surgery 14 patients had a positive and 4 a negative test result. No complication occurred during the test performed early after surgery. Of the 14 patients with positive dipyridamole echocardiographic results before surgery, 10 had negative and 4 had positive results after surgery. All 4 patients had negative results before and after surgery. In the 4 patients with positive results after dipyridamole echocardiographic testing before and after bypass surgery, dipyridamole time increased from 5.8 ± 5 to 9.3 ± 0.9 minutes (p = 0.3) after the procedure and wall motion score index at peak dipyridamole changed from 1.55 ± 0.2 to 1.28 ± 0.3 (p = 0.05). Forty-nine of 53 grafts were patent as seen on angiography. Dipyridamole echocardiographic results were positive in 4 of 5 patients who had at least 1 obstructed graft or native vessel obstructed distal to bypass graft insertion. The remaining patient had diagnostic electrocardiographic changes during dipyridamole infusion without wall motion abnormalities. Dipyridamole echocardiographic results were negative in all 13 patients who had complete revascularization. In the 4 patients with positive test results, the procedure correctly identified the localization of the diseased bypass graft. These data suggest that (1) dipyridamole echocardiography can be easily and safely performed after coronary artery bypass graft surgery, (2) there is an excellent correlation between the functional improvement assessed by dipyridamole echocardiography testing and anatomic results of coronary artery bypass surgery, and (3) it reliably detects and identifies diseased bypass grafts.

Prevalence of undiagnosed chronic thromboembolic pulmonary hypertension after pulmonary embolism.

Chronic thromboembolic pulmonary hypertension is associated with adverse prognosis. Early diagnosis is important to better identify patients who would benefit from a well established therapeutic strategy. The purpose of our study was to evaluate long-term incidence of undiagnosed chronic thromboembolic pulmonary hypertension after acute pulmonary embolism and the utility of a long-term follow-up including an echocardiographic-based screening programme to early detect this disease. We evaluated retrospectively 282 patients discharged from the ‘Maggiore della Carità’ Hospital, Università del Piemonte Orientale, Novara, Italy, with diagnosis of acute pulmonary embolism between November 2006 and October 2009. One hundred and eleven patients underwent a clinical late echocardiographic screening programme after the acute event. Patients with suspected pulmonary hypertension based on echocardiographic evidence of systolic pulmonary artery pressure of at least 40 mmHg underwent complete work-up for chronic thromboembolic pulmonary hypertension assessment, including ventilation-perfusion lung scintigraphy and right heart catheterization.One hundred and eleven patients were included in the study. Pulmonary hypertension was suspected in 15 patients; five patients had chronic thromboembolic pulmonary hypertension confirmed by ventilation-perfusion lung scintigraphy, right heart catheterization and pulmonary angiography. Two patients with clinical class functionally advanced underwent surgical pulmonary endarterectomy and two asymptomatic patients underwent medical treatment. The prevalence of undiagnosed chronic thromboembolic pulmonary hypertension was 4.5%.Chronic thromboembolic pulmonary hypertension is a serious disease with a poor prognosis if not treated early. Surgical treatment is decisive. After surgery, the majority of patients have a substantial improvement in their functional status and in haemodynamic variables. Many patients are asymptomatic. Implementation of screening programmes may be helpful for an early diagnosis and early proper therapy.

Left ventricular torsion in paced patients.

Background In healthy people the left ventricle presents a counter-clockwise apical rotation and a clockwise basal rotation ending in late systole. In early systole (during isovolumic contraction) there is a fast and inverse rotation (counter-clockwise at the base and clockwise at the apex). This opposite rotation between apex and base produces the systolic torsion of the left ventricle. The effect of permanent conventional pacing on this torsion is little known. Objectives The aim of this study was to assess, by speckle tracking echocardiography, left ventricular rotation and torsion in patients conventionally paced at the apex of the right ventricle. Methods Left ventricular apical and basal rotation and the consequent torsion were evaluated by means of speckle tracking echocardiography, in 13 paced patients, without ischemic or valvular disease, and in 17 healthy participants. Left ventricular dyssynchrony was evaluated by means of temporal uniformity of strain. Results In the paced group there was a significant reduction in early-systolic clockwise torsion (−0.4° ± 1.2 vs. −1.5° ± 1.6; P = 0.04), and in late-systolic counter-clockwise torsion (15.1° ± 4.3 vs. 19.1° ± 5.5; P = 0.03). Circumferential temporal uniformity of strain averaged significantly lower in paced patients. Conclusions Conventional pacing from the apex of the right ventricle alters both the torsional mechanic and the synchrony of the left ventricle.

Comparison between IEGM-based approach and echocardiography in AV/PV and VV delay optimization in CRT-D recipients (Quicksept study)

Background AtrioVentricular (AV) and InterVentricular (VV) delay optimization can improve ventricular function in Cardiac Resynchronization Therapy (CRT) and is usually performed by means of echocardiography. St Jude Medical has developed an automated algorhythm which calculates the optimal AV and VV delays (QuickOpt™) based on Intracardiac ElectroGrams, (IEGM), within 2 min. So far, the efficacy of the algorhythm has been tested acutely with standard lead position at right ventricular (RV) apex. Aim of this project is to evaluate the algorhythm performance in the mid- and long-term with RV lead located in mid-septum. Methods AV and VV delays optimization data were collected in 13 centers using both echocardiographic and QuickOpt™ guidance in CRTD implanted patients provided with this algorhythm. Measurements of the aortic Velocity Time Integral (aVTI) were performed with both methods in a random order at pre-discharge, 6-month and 12-month follow-up. Results Fifty-three patients were studied (46 males; age 68 ± 10y; EF 28 ± 7%). Maximum aVTI obtained by echocardiography at different AV delays, were compared with aVTI acquired at AV delays suggested by QuickOpt. The AV Pearson correlations were 0.96 at pre-discharge, 0.95 and 0,98 at 6- and 12- month follow-up respectively. After programming optimal AV, the same approach was used to compare echocardiographic aVTI with aVTI corresponding to the VV values provided by QuickOpt. The VV Pearson Correlation were 0,92 at pre-discharge, 0,88 and 0.90 at 6-month and 12- month follow-up respectively. Conclusions IEGM-based optimization provides comparable results with echocardiographic method (maximum aVTI) used as reference with mid-septum RV lead location.

Angiographic Correlates of Different Mechanical Effects During the Dipyridamole Echocardiography Test Shortly After Acute Myocardial Infarction

The aim of this study was to analyze the different mechanical patterns during the dipyridamole echocardiography test (DET) performed in 167 patients 8–10 days after a first myocardial infarction. The results were correlated with coronary angiography. In a first series of 98 patients retrospectively analyzed (group I), four different types of dipyridamole‐induced wall‐motion abnormalities were observed: (1) worsening of wall motion in the same region showing asynergy at rest (type I); (2) new wall‐motion abnormality in a territory adjacent to the resting asynergies and fed by the same vessel (type II); (3) new wall‐motion abnormality in a territory adjacent to the resting asynergies, but supplied by a vessel different from the infarct related artery (type III); and (4) new wall‐motion abnormality not directly adjacent to the infarct zone (type IV). Type IV asynergies were found in one of 44 patients with single vessel disease and in 14 of 54 patients with multivessel disease (sensitivity 70.4%, specificity 92.3%). Type III asynergies developed in two patients with single vessel disease and in 24 of those with multivessel disease. The frequency and distribution of the four asynergy types were subsequently analyzed in a second prospective series of 69 patients (group II). Type III and IV asynergies were found almost exclusively in patients with multivessel disease (17/34 patients with multivessel disease and 2/35 with single vessel disease) (sensitivity 50%, specificity 94.3%). Combining type III and IV asynergies, an overall sensitivity of 62% and a specificity of 94% for predicting multivessel disease were obtained. The ability of DET to predict specific vessel obstruction was also investigated. A positive correlation was found only for the laterobasal segment (specificity 82% in predicting critical stenosis of the left circumflex artery [LCX]), and for the apical and distal septal segments (specificity 95% and 93% for lesions of the left anterior descending artery [LAD], respectively). A substantial overlap was noted when an attempt was made to distinguish LCX from right coronary artery (RCA) lesions. Nevertheless, new simultaneous wall‐motion abnormalities of the posterobasal septal and laterobasal segments were observed in all but one patient with combined lesions of LCX and RCA (specificity 99%). In conclusion, the mechanical patterns of dipyridamole‐induced new wall‐motion abnormalities correlate with coronary angiography: new remote asynergies are highly specific in predicting multivessel disease, but are not frequent. New asynergies adjacent to the infarct zone can also predict multivessel disease, provided they are located in a different vascular region. The ability of DET to predict specific vessel obstructions was excellent for LAD lesions, but it was less helpful in differentiating LCX from RCA lesions. Nevertheless, new simultaneous wall‐motion abnormalities of the posterobasal septal and laterobasal wall predict critical lesions of the LCX and RCA.

Dipyridamole-echocardiography: clinical usefulness following interventions.

Dipyridamole‐echocardiography test response can be expressed not only in a black or white (positive vs negative) code but also, in positive tests, by a gray scale integrating the severity and extent of the dyssynergy as well as the ischemia‐free stress time. The recognition of the dyssynergy is important to establish the diagnosis; however, the evaluation of the degree of the induced ischemia, stratified according to spatiotemporal coordinates, is even more important because it accurately predicts the coronary anatomical and functional situation, as well as the prognosis of the individual patient. Furthermore, the “shades of gray” in a positive response have proved useful in assessing the beneficial effects of several interventions: coronary angioplasty; coronary artery bypass surgery; thrombolysis; and medical antianginal therapy. Due to its excellent reproducibility, dipyridamole‐echocardiography can play a pivotal role for simple, safe, fast, accurate, and objective assessment of therapeutic interventions, either mechanical or pharmacological, based upon the presence, timing, severity, and extent of dipyridamole‐induced dyssynergy.