Biomedical subjects
Publications and source records attributed to Giuseppe Tarantini.
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The aim of this study was to evaluate the impact of age on immediate- and long-term outcomes of percutaneous mitral balloon valvuloplasty (PMV). PMV is the first-line treatment for patients with symptomatic mitral stenosis. However, long-term results in large series of patients from Europe and the United States have been found less favorable than those from Asia and South America involving younger patients. Six hundred ten patients who underwent 626 PMV procedures were prospectively followed for 6.1 +/- 4.10 years using clinical and echocardiographic evaluation. Patients were divided in quartiles according to age: < or =41 years (n = 163), 42 to 53 years (n = 163), 54 to 63 years (n = 142), and >63 years (n = 158). The success of PMV was defined as valve area > or =1.5 cm(2) without severe regurgitation; restenosis was defined as a loss > or =50% of initial gain, with a valve area of <1.5 cm(2). PMV success was significantly more prevalent in younger patients: 95.7% in group 1, 91.4% in group 2, 86.4% in group 3, and 83.4% in group 4 (p = 0.002). No significant differences in complications were found among all age groups, including death, cardiac tamponade, emergency mitral replacement, and any embolic events (p = NS). Event-free survival was greater in younger patients (p <0.0001), but on multivariate analysis, age was not an independent predictor of events (p = NS). Restenosis occurred in 27.9% of patients, throughout all groups (p = NS). In conclusion, PMV may be safely and effectively performed in younger and older patients. Although event-free survival was greater in younger groups, multivariate analysis did not find that age was an independent predictor of events.
Infarct size has been considered an established marker of left ventricular (LV) remodeling. We assessed the predictive value of myocardial/microvascular injury assessed by delayed enhanced magnetic resonance imaging (MRI) on LV remodeling and LV ejection fraction after primary coronary intervention (PCI) compared with peak troponin levels, an established index of myocardial infarct size. We performed MRI in 76 patients with first acute myocardial infarction 6 +/- 2 days after successful PCI. Necrosis was judged as transmural when delayed enhancement was extended to >or=75% of LV segment thickness. Severe microvascular obstruction was identified as areas of late hypoenhancement surrounded by delayed enhancement. Infarct size was expressed as an index by dividing the total percentage of delayed enhancement involvement by the number of LV segments. LV end-diastolic volume index and function were quantified by 2-dimensional echocardiography at 6 +/- 1 months after acute myocardial infarction. Remodeling was evaluated as a change in LV end-diastolic volume index at follow-up compared with baseline. At univariate analyses, transmural necrosis, severe microvascular obstruction, infarct size, and troponin level were correlated directly with remodeling and inversely with LV function at follow-up (p <0.001). At multiple regression, only transmural necrosis and troponin level remained independent predictors of LV remodeling and function. With respect to troponin, transmural necrosis improved the predictive power of LV remodeling (R2 for change = 0.19) and function (R2 for change = 0.16). In conclusion, in patients with acute myocardial infarction undergoing PCI, the amount of transmural necrosis as assessed by MRI is a major determinant of LV remodeling and function, with significant additional predictive value to infarct size and severe microvascular obstruction.
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BACKGROUND: Administration of L-carnitine in patients with anterior acute myocardial infarction (AMI) prevents left ventricular remodeling. Current study was aimed to assess the effect of L-carnitine administration on mortality and heart failure in patients with anterior AMI. METHODS: CEDIM 2 trial was a randomized, double-blind, multicenter, placebo-controlled trial planned to enroll 4,000 patients with acute anterior AMI. The trial was interrupted after the enrolment of 2,330 patients because of the lower than expected enrolment rate. The primary end point was a composite of death and heart failure at 6 months; 5-day mortality was the secondary end point. RESULTS: During the 6-month follow-up, the primary end-point was not significantly different between the L-carnitine and placebo group (9.2 vs. 10.5%, p = 0.27). A reduction in mortality was seen in the L-carnitine arm on day 5 (secondary end-point) from randomization (HR = 0.61, 95% CI 0.37-0.98, p = 0.041). CONCLUSIONS: In CEDIM 2 trial L-carnitine therapy led to a reduction in early mortality (secondary end-point) without affecting the risk of death and heart failure at 6 months in patients with anterior AMI, leading to a non-significant finding with respect to the primary end-point.
Patients with multivessel coronary artery disease and severe left ventricular dysfunction are considered to be at high risk for percutaneous coronary intervention, and often are poor surgical candidates because of severe comorbidity. We report a case of high-risk percutaneous coronary intervention in a 67-year-old man with a severe left ventricular dysfunction and three-vessel coronary artery disease using a novel left ventricular assist device.
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Our study evaluated the interaction across mortality risk, time delay related to percutaneous coronary intervention (PCI), and survival benefit of PCI over thrombolytic therapy (risk-time benefit analysis). Mortality risk and angioplasty-related time delay were independently correlated to 30-day survival benefit of primary angioplasty over lytic therapy. A PCI-related delay>60 minutes could be justified for high-risk patients.
OBJECTIVES: This study sought to assess the relationship between duration of ischemia and both myocardial transmural necrosis (TN) and severe microvascular obstruction (SMO), by contrast-enhanced magnetic resonance (CE-MR), in patients with acute myocardial infarction (AMI) treated with angioplasty (PCI), and to estimate the risk of TN and SMO with the duration of ischemia. BACKGROUND: The impact of ischemic time on myocardial and microvascular injury is not well characterized in people. METHODS: We performed CE-MR in 77 patients with first AMI, 5 +/- 3 days after successful PCI. The AMI was labeled as transmural if hyperenhancement at CE-MR was extended to > or =75% of the thickness in two or more ventricular segments. The SMO was identified as areas of late hypoenhancement surrounded by hyperenhanced tissue. The relationship between ischemic time and CE-MR evidence of SMO or TN was evaluated by logistic regression. RESULTS: Thirteen patients were excluded because of preprocedural Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 of the infarct-related artery. For the remaining 64 patients, the mean time to treatment was 190 +/- 110 min, 45 (65%) patients had TN and 23 (39%) had SMO. Mean pain to balloon time was 90 +/- 40 min, 110 +/- 107 min, and 137 +/- 97 min in patients without TN and SMO, with TN but without SMO, or with both TN and SMO, respectively (p = 0.001). Multivariate analysis showed that time delay was significantly associated both with TN (odds ratio per 30 min, 1.37, p = 0.032), and SMO (odds ratio per 30 min, 1.21; p = 0.021). CONCLUSIONS: In AMI patients with impaired coronary perfusion undergoing PCI, the risk of TN and SMO increases with the duration of the ischemic time.
BACKGROUND: The outcome of moderate-to-severe ischemic mitral regurgitation with multivessel coronary artery disease is still debated. We analysed the effect of different treatments, i.e. medical therapy (MT), coronary artery by-pass grafting (CABG) alone and CABG with mitral valve surgery (MVS), on the survival and rehospitalization of these patients. METHODS: Between 1990 and 2002, we identified 111 consecutive patients, aged 73+/-8 years, with chronic moderate-to-severe mitral regurgitation and multivessel coronary artery disease at cardiac catheterization, in absence of primary valve disease. Twenty-two patients were treated by MT, 50 by CABG and 39 by CABG+MVS. Overall, the median clinical and echocardiographic follow-ups were 34.9 and 14.6 months, respectively. RESULTS: Groups differed significantly (p < 0.03) for left ventricular end-diastolic volume index (MT 153+/-54, CABG 125+/-35, CABG + MVS 129+/-38, ml/m2), ejection fraction (MT 35+/-14, CABG 38+/-13, CABG + MVS 50+/-14, %) and mammary artery graft use (CABG 60, CABG + MVS 74, %). While in-hospital mortality was higher in surgical patients (MT 13.6, CABG 18, CABG + MVS 17.9, %, p=0.09), 7-years mortality showed a trend in favour of CABG + MVS compared to other groups (MT 100, CABG 57, CABG + MVS 29, %, p = 0.1). After adjusting for baseline differences, CABG alone or with MVS had a 57% (HR 0.43, p = 0.005) and 53% (HR 0.47, p = 0.02) risk reduction of combined cardiac death and rehospitalization rate compared to MT. However, only CABG + MVS independently predicted mortality (risk reduction 65%, HR 0.35, p = 0.027). CONCLUSIONS: In moderate-to-severe ischemic mitral regurgitation and multivessel coronary artery disease, surgery reduced total cardiac events but only a concomitant MVS significantly improved survival.
BACKGROUND: Three-dimensional electroanatomic voltage mapping offers the potential to identify low-voltage areas that correspond to regions of right ventricular (RV) myocardial loss and fibrofatty replacement in patients with arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). METHODS AND RESULTS: Thirty-one consecutive patients (22 men and 9 women; mean age, 30.8+/-7 years) who fulfilled the criteria of the Task Force of the European Society of Cardiology and International Society and Federation of Cardiology (ESC/ISFC) for ARVC/D diagnosis after noninvasive clinical evaluation underwent further invasive study including RV electroanatomic voltage mapping and endomyocardial biopsy (EMB) to validate the diagnosis. Multiple RV endocardial, bipolar electrograms (175+/-23) were sampled during sinus rhythm. Twenty patients (group A; 65%) had an abnormal RV electroanatomic voltage mapping showing > or =1 area (mean 2.25+/-0.7) with low-voltage values (bipolar electrogram amplitude <0.5 mV), surrounded by a border zone (0.5 to 1.5 mV) that transitioned into normal myocardium (>1.5 mV). Low-voltage electrograms appeared fractionated with significantly prolonged duration and delayed activation. In 11 patients (group B; 35%), electroanatomic voltage mapping was normal, with preserved electrogram voltage (4.4+/-0.7 mV) and duration (37.2+/-0.9 ms) throughout the RV. Low-voltage areas in patients from group A corresponded to echocardiographic/angiographic RV wall motion abnormalities and were significantly associated with myocyte loss and fibrofatty replacement at EMB (P<0.0001) and familial ARVC/D (P<0.0001). Patients from group B had sporadic disease and histopathological evidence of inflammatory cardiomyopathy (P<0.0001). During the time interval from onset of symptoms to the invasive study, 11 patients (55%) with electroanatomic low-voltage regions received an implantable cardioverter/defibrillator because of life-threatening ventricular arrhythmias, whereas all but 1 patient with a normal voltage map remained stable on antiarrhythmic drug therapy (P=0.02). CONCLUSIONS: Three-dimensional electroanatomic voltage mapping enhanced accuracy for diagnosing ARVC/D (1) by demonstrating low-voltage areas that were associated with fibrofatty myocardial replacement and (2) by identifying a subset of patients who fulfilled ESC/ISFC Task Force diagnostic criteria but showed a preserved electrogram voltage, an inflammatory cardiomyopathy mimicking ARVC/D, and a better arrhythmic outcome.
The annual incidence of stroke in patients with nonrheumatic atrial fibrillation averages 5% per year and increases with age, left ventricular dysfunction, hypertension, diabetes or prior stroke. Since in nonrheumatic atrial fibrillation 91% of left atrial thrombi are located in the left atrial appendage, in patients ineligible for oral anticoagulation it was suggested the percutaneous closure of left atrial appendage as a therapeutic option to reduce embolic risk. In this article we report our initial experience with this procedure, which was uneventful and efficacious at short-term follow-up. In conclusion, the interventional approach in patients with atrial fibrillation ineligible for oral anticoagulation seems feasible and promising, and deserves further investigation.
We sought to evaluate myocardial reperfusion and its prognostic value after percutaneous transluminal coronary angioplasty (PTCA) in patients admitted for cardiogenic shock. Lack of myocardial reperfusion despite restored coronary flow affects the survival of patients with acute myocardial infarction (AMI). Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We assessed MBG in 41 consecutive patients admitted to our department within 12 hours from the onset of AMI and in cardiogenic shock. PTCA was successful in 83% of patients. Thrombolysis In Mycardial Infarction (TIMI) grade 3 flow was demonstrated in 22 patients (53%). MBG 2/3 was found in 14 patients (34%); among them, 12 had TIMI 3 flow. Compared with patients with MBG 2/3, those with MBG 0/1 were older (71 +/- 11 vs 57 +/- 13 years, p = 0.001), had a higher prevalence of diabetes (48% vs 14%, p = 0.04) and hypertension (63% vs 29%, p = 0.04), showed a trend toward longer ischemic time (6.1 +/- 2.4 vs 4.9 +/- 1.1), and had larger enzymatic infarct size (peak creatine kinase 7,690 +/- 3,516 vs 5,500 +/- 2,977 IU/L). Mortality was higher in patients with MBG 0/1 both in the hospital (81% vs 14%, p <0.001) and at follow-up (81% vs 29%, p = 0.001). After adjustment by multivariate analysis, MBG 0/1 (odds ratio 16, p = 0.01) and age (odds ratio 3.8/10 years, p = 0.04) were correlated with in-hospital mortality. MBG 2/3 was achieved in a few patients in cardiogenic shock after AMI who were treated with PTCA; this was a strong predictor of in-hospital survival. Also, risk stratification after mechanical revascularization should include assessment of restoration of myocardial reperfusion.
Ths study reports different mechanisms (i.e., microvascular spasm and discrete microinfarction) that may underlie different pattern of slow-reflow after elective coronary stenting on the basis of the different tissue level of perfusion achieved, assessed by blush grade and MRI.
BACKGROUND: There is very little known about the relationship between pre-intervention arterial pressure response to vasopressor therapy (PRV) and death rate, after primary angioplasty for immediate cardiogenic shock (CS) complicating acute myocardial infarction (AMI). METHODS: We examined data from 32 consecutive cases, admitted to our department within 12 h after the onset of MI and in CS, treated with direct PTCA, from May 1995 to March 2001. Intravenous administration of dobutamine and vasopressor agents was required in all patients before intervention. RESULTS: Ten patients, after vasopressor therapy, showed a significant improvement in systolic arterial pressure, invasively measured, (>90 mmHg, responders) before undergoing PTCA. Responders were younger and with less impaired pre-procedural LVEF (39.6%+/-10.7 vs. 30.9%+/-8.4, P=0.02). After direct PTCA responders showed an improved final TIMI flow (2.8+/-0.6 vs. 2.2+/-0.7, P=0.04) and blush grade (1.9+/-0.9 vs. 1+/-1, P=0.03). The mortality rate was lower in responders compared with non-responders both in hospital (20% vs. 68%, P=0.02) and at 3.5 years of follow-up (30% vs. 73%, P=0.049). After adjustment by multivariate analysis older age and lower blush grade correlated with in hospital death, while age remained the only predictor of late death. CONCLUSIONS: PRV was not an independent predictor of death after direct PTCA for CS. The association of no PRV with older age and lower post procedural blush grade may explain the difference in mortality rates between responders and non-responders.
BACKGROUND: Ventriculo-arterial coupling, defined as the ratio of the effective afterload (Ea) to contractility (Ees), reflects the mechano-energetic performance of the heart and is increased in chronic heart failure (CHF); the aim of treatment is to reduce its value. We studied the effect of carvedilol on the Ea/Ees ratio in patients with CHF treated with ACE-inhibitors, diuretics, and digoxin. METHODS: Between November 1999 and October 2001, 36 consecutive ambulatory patients (aged 31 to 76 years) with stable CHF and idiopathic or hypertensive cardiomyopathy, in sinus rhythm and with a left ventricular ejection fraction < or = 40%, were started on carvedilol and the dose was increased to the maximum tolerated. Ees was calculated as the left ventricular systolic pressure--taken as the systolic arterial pressure measured using the cuff manometer simultaneously with two-dimensional echocardiographic recordings--divided by the left ventricular end-systolic volume. Ea was measured as the ratio of the left ventricular systolic pressure to the stroke volume. All patients were investigated prospectively after 6 and 12 months of treatment. RESULTS: Out of 36 patients, 4 did not tolerate the drug and were dropped out. At 6.35 +/- 1 months, the daily dosage of carvedilol was 49.7 +/- 21 mg. The NYHA functional class improved from 1.52 +/- 0.67 to 1.29 +/- 0.53 (p = 0.017), the heart rate markedly diminished from 73.6 +/- 13.3 to 60.8 +/- 10.8 b/min (p < 0.001) and so did Ea (3.35 +/- 0.91 to 2.84 +/- 0.93, p = 0.001). Peripheral resistances and Ees did not change. Therefore, the decrease in the Ea/Ees ratio (2.61 +/- 0.78 vs 2.19 +/- 0.89, p = 0.004) and the related increase in left ventricular ejection fraction (28.8 +/- 5.68 vs 33.3 +/- 7.5%, p < 0.001) were due to the decrease in Ea, while Ees did not vary significantly. Moreover, the Ea reduction was related linearly to the decrease in heart rate (r = 0.46, p = 0.001). There was no change in diuretic or ACE-inhibitor dosing during carvedilol titration. At 14.7 +/- 2 months of follow-up, no further variation occurred, short of a trend toward a slight increase in Ees (1.38 +/- 0.49 to 1.58 +/- 0.65, p = 0.07). CONCLUSIONS: Carvedilol, added to the conventional therapy of CHF, improves left ventricular performance and reduces the Ea/Ees ratio by decreasing Ea, mainly through a reduction in heart rate. This effect is already evident at 6 months and persists later on, while only after 12 months does Ees tend to increase slightly.
BACKGROUND: The time-to-treatment is a critical determinant of outcome after acute myocardial infarction. We investigated the relationship between the primary angioplasty (PCI)-related time delay and the benefit of PCI over thrombolytic therapy (TT), considering the time elapsing from symptom onset in 21 randomized trials comparing PCI to TT. METHODS: PCI-related time delay was calculated as the median of the "door-to-balloon" time minus the median of the "door-to-needle" time. The survival benefit was defined as the difference between 30-day mortality after TT and after PCI. The relationships between time delay and benefit were assessed by linear regression. RESULTS: PCI-related time delay ranged from 7 to 104 min. Linear regression showed that at a PCI-related delay of 75 min, PCI and TT yielded equivalent reductions in mortality (p = 0.03). When the trials with the longest and shortest delays were excluded, the benefit of PCI over TT was nullified after a delay of 62 min, and every additional 10-min delay produced a 1.1% increase in mortality (p = 0.01). When trials with a symptom duration < 6 hours (median 130 min) were considered, PCI-related delay still correlated with an absolute risk reduction in 30-day mortality with a time to equipoise of 57 min (p = 0.03). Lack of correlation (p = 0.85) was observed in trials enrolling patients within 12 hours of symptom onset (median 185 min). CONCLUSIONS: Our analysis suggests that PCI-related delay substantially modifies the benefit of PCI over TT, particularly in case of patients presenting early following symptom onset.