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F Crea

Publications and source records attributed to F Crea.

At least 109 records · Page 6Linked to original sources
PubMed1996

Electrograms for identification of the atrial ablation site during catheter ablation of accessory pathways.

BACKGROUND: Catheter ablation of accessory pathways using radiofrequency current has been shown to be effective in patients with Wolff-Parkinson-White syndrome, by using either the ventricular or atrial approach. However, the unipolar electrogram criteria for identifying a successful ablation at the atrial site are not well established. METHODS AND RESULTS: One hundred patients with Wolff-Parkinson-White were treated by delivering radiofrequency energy at the atrial site. Attempts were considered successful when ablation (disappearance of the delta wave) occurred in < 10 seconds. In eight patients with concealed pathway, the accessory pathway location was obtained by measuring the shortest V-A interval either during ventricular pacing or spontaneous or induced reciprocating tachycardia. In 92 patients both atrioventricular valve annuli were mapped during sinus rhythm, in order to identify the accessory pathway (K) potential before starting the ablation procedure. When a stable filtered (30-250 Hz) "unipolar" electrogram was recorded, the following time intervals were measured: (1) from the onset of the atrial to the onset of the K potential (A-K); (2) from the onset of the delta wave to the onset of the K potential (delta-K); and (3) from the onset of the K potential to the onset of the ventricular deflection (K-V). During unsuccessful versus successful attempts, A-K (51 +/- 11 ms vs 28 +/- 8 ms, P < 0.0001 for left pathways [LPs]; and 44 +/- 8 ms vs 31 +/- 8 ms, P < 0.02 for right pathways [RPs]) and delta-K intervals (2 +/- 9 ms vs -18 +/- 10 ms, P < 0.0001 for LPs; and 13 +/- 7 ms vs 5 +/- 8 ms, P < 0.02 ms for RPs) were significantly longer. CONCLUSIONS: Short A-K interval (< 40 ms), and a negative delta-K interval recorded from the catheter positioned in the atrium are strong predictors of successful ablation of LPs and RPs. Therefore, the identification of the K potential appears to be of paramount importance for positioning of the ablation catheter, followed by analysis of A-K and delta-K unipolar electrogram intervals. However, it appears that the mere recording of K potential is not, per se, predictive of successful outcome, but rather the A-K and delta-K interval.

Adolescent↗
PubMed1996

[Transcatheter radiofrequency ablation in supraventricular tachycardia in children: immediate results and mid-term follow-up].

OBJECTIVES: The purpose of this study was to evaluate the efficacy and safety of radiofrequency ablation of supraventricular tachycardias due to a reentry circuit in a group of closely followed-up pediatric patients. PATIENTS: Forty-six pediatric patients (mean age 12.6 years, range 3-18) underwent a total of 48 radiofrequency ablation procedures for reciprocating supraventricular tachycardia. Thirty-nine had an orthodromic reentry tachycardia, 6 an atrioventricular node reentry tachycardia and 1 a permanent junctional reciprocating tachycardia. METHODS: To ablate the overt accessory pathways, the Kent potential (K) was identified and then the shortest A-K, and delta wave-K intervals were measured. The shortest V-A interval was identified for those concealed. For the left-sided accessory pathways, we used the retrograde transaortic approach in 10 procedures and the transseptal approach in 18. Atrioventricular node reentry tachycardia was ablated at the site where the slow-pathway electrogram was recorded. Follow-up clinical data, electrocardiogram, 24-hours Holter monitoring and transesophageal atrial stimulation were obtained and evaluated. RESULTS: Early: We performed a total of 48 procedures. Among 41 procedures performed in the 39 patients with accessory pathway, 38 were successful (92,6%). Mean fluoroscopy time was 31 +/- 18 min. For left sided accessory pathways, mean fluoroscopy time of procedures with retrograde approach was 45 +/- 10 min and with transseptal 23 +/- 12 min (p < 0.01). Ablation of slow-pathway in patients with intranodal reentry tachycardia was successful in 3/6 cases (50%). The patient with permanent junctional reciprocating tachycardia was successfully ablated. Late: All patients are alive and none was lost during the follow-up after a mean time of 12.9 months (range 5-33). Success at last follow-up was 100% in patients with an accessory pathway and 33% in patients with atrioventricular node reentry. In patient with permanent junctional reciprocating tachycardia, the arrhythmia appeared again one month after the procedure, thus a second successful attempt was performed. COMPLICATIONS: Major complications (6,5%) including a right femoral vein thrombosis (one patient), an hematoma without pulse loss (one patient) and a non-sustained monomorphic ventricular tachycardia (one patient). CONCLUSIONS: Our data show high efficacy of radiofrequency ablation in pediatric patients with accessory pathways. The risks are low at follow-up evaluation, but might be helpful a longer-term follow-up in order to evaluate the risk of a long fluoroscopy time and the arrhythmogenic effect of the scar.

Adolescent↗
PubMed1996

[Beans and infarct].

Explore the source record for details and available documents.

Coronary Artery Disease↗
PubMed1995

Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris, and in acute myocardial infarction.

Coronary angiographic findings were compared in patients who presented with acute myocardial infarction (AMI, n = 75), unstable angina pectoris (UAP, n = 36), or stable angina pectoris (SAP, n = 36) for > or = 2 years without evidence of any previous acute event and with an angiogram within 2 years of the initial symptoms. Angiograms were evaluated blindly for severity, extent (depending on the percentage of each coronary segment showing atherosclerosis), and pattern (discrete, < 3 loci of narrowings involving < 50% of any segment; diffuse, anything exceeding this). Patients in the SAP group had more narrowed arteries (2.4 +/- 0.7 vs 1.3 +/- 0.6 [p < 0.02] and 1.4 +/- 0.6 [p < 0.02]), more stenoses (6.0 +/- 3.3 vs 2.1 +/- 1.5 [p < 0.01] and 2.6 +/- 1.7 [p < 0.05]) and occlusions (1.3 +/- 1.1 vs 0.7 +/- 0.6 [p = 0.05] and 0.3 +/- 0.5 [p < 0.02]), and a greater extent index (0.9 +/- 0.5 vs 0.5 +/- 0.3 [p < 0.02] and 0.5 +/- 0.3 [p < 0.02]) than those in the AMI and UAP groups. Furthermore, a discrete pattern was less prevalent in patients with UAP than in those with SAP or AMI (3% vs 40% [p < 0.02] and 25% [p < 0.05], respectively). In conclusion, patients who present with acute coronary syndromes have less extensive atherosclerosis than those who present with chronic stable angina. Therefore, in the former group, coronary atherosclerosis appears to be more susceptible to ischemic stimuli responsible for acute coronary syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1995

Circadian variation of ischemic threshold in syndrome X.

To evaluate whether the ischemic threshold has a circadian rhythm in patients with syndrome X, we analyzed 90 episodes of ST depression detected on 24-hour Holter recordings of 12 such patients. Ischemic threshold was considered as heart rate (HR) at 1 mm ST depression. To correct for differences in basal HR among patients, however, the ischemic threshold was also calculated as a normalized index of HR at 1 mm ST depression: [(HR at 1 mm ST-24-hour modal HR)/24-hour modal HR]-100. Mean hourly values of both absolute and normalized HRs at 1 mm ST depression were obtained by grouping and averaging respective values of all episodes detected in every hour of the day in all patients. Chronobiologic analysis was performed by single cosinor method. A significant circadian rhythm was found for HR (mesor 76 beats/min, amplitude 10 beats/min, acrophase at 2:16 P.M., p < 0.001), number of episodes of ST depression (mesor 3.75, amplitude 2.9, acrophase at 2:45 P.M., p < 0.001) and cumulative time of ischemia, with a high correlation of distributions. Episodes of ST depression showed a double peak initially in the morning, and again in the afternoon. Both raw and normalized values of HR at 1 mm ST depression also had a significant circadian variation in ischemic threshold, which was lower in the night and early morning hours, progressively increased until the first afternoon hours, and subsequently decreased in the evening.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Cytomegalovirus replication is not a cause of instability in unstable angina.

BACKGROUND: Unstable angina is most frequently caused by coronary thrombosis, with or without plaque fissure, but the mechanisms underlying these events are still speculative. Since cytomegalovirus (CMV) antigens and DNA encoding CMV major immediate-early (MIE) gene have been detected in atherosclerotic arterial walls, the active replication of CMV may be responsible for plaque instability. Therefore the expression of CMV MIE gene mRNA, an early marker of viral replication, was assessed in coronary atherectomy specimens from patients with stable or unstable angina. METHODS AND RESULTS: Twenty patients with unstable angina (12 men and 8 women; mean age, 62 years; range, 44 to 89 years) and 20 patients with stable angina (16 men and 4 women; mean age, 62 years; range, 43 to 81 years) who underwent successful directional coronary atherectomy were enrolled in the study. The efficiency of mRNA extraction, transcription, and amplification from each coronary atherectomy specimen was assessed by performance of reverse transcription and thermal cycling amplification of a 548-bp human beta-actin cDNA segment. After Southern blotting and hybridization with a specific probe, all specimens but one showed a positive hybridization signal. The negative sample was excluded from the study. Reverse transcription and thermal cycling amplification of a 145-bp CMV cDNA segment of the MIE gene were then carried out. After Southern blotting and hybridization with a specific probe, none of the specimens showed a positive hybridization signal. Plasmid pACYC 184 containing the Xba I-inserted MIE gene cDNA was used as a positive control: as few as 10 molecules of the plasmid per reaction were detectable after amplification. CONCLUSIONS: Our results do not support the hypothesis that, in patients with unstable angina, replication of CMV in coronary atherosclerotic plaques is a major cause of plaque instability. These findings suggest that the research for the causes of unstable angina should be directed toward processes other than CMV replication.

Angina Pectoris↗
PubMed1995

Relation between myocardial infarction site and pain location in Q-wave acute myocardial infarction.

Location, severity, duration, and time course of pain were assessed in 104 consecutive patients with either first or second, anterior or inferior Q-wave acute myocardial infarction (AMI). Pain severity was assessed using a visual analog scale. Pain location and radiation were similar in 48 patients with anterior and 56 patients with inferior wall AMI. Pain duration (6.1 +/- 6.4 vs 6.5 +/- 5.4 hours, p = NS) and severity (68 +/- 21 vs 61 +/- 21 mm, p = NS) were also similar. The pain was continuous in 34 patients with anterior (71%) and in 42 with inferior (75%) wall AMI. Among the 41 patients who did not receive thrombolytic therapy, 18 patients with continuous pain had a higher creatine kinase peak level than the remaining 23 patients with intermittent pain or preinfarction angina, or both (2,065 +/- 1,017 vs 1,162 +/- 994 IU, p < 0.01). The incidence of gastrointestinal symptoms was slightly higher in patients with inferior than anterior wall AMI (70% vs 48%, p < 0.05). Among 32 patients admitted with a second AMI, pain location was similar in 14 who had both infarcts in the same myocardial region, but was different in 12 of 18 (67%) who had a first and second infarct in different regions (p < 0.001). Thus, patients with anterior or inferior wall AMI experienced pain in similar body regions. However, in patients who presented with > 1 AMI, different locations of the infarction pain were highly predictive of ischemia occurring in different myocardial regions. Finally, patients with preinfarction angina or intermittent pain tended to have smaller infarcts.

Adult↗
PubMed1995

Muscular and cardiac adenosine-induced pain is mediated by A1 receptors.

OBJECTIVES: This study attempted to establish whether bamiphylline, a selective antagonist of A1 adenosine receptors, prevents the algogenic effects of adenosine in humans. BACKGROUND: Experimental findings indicate that the sympathoexcitatory response elicited by adenosine is mediated by A1 receptors. METHODS: An intrailiac infusion of increasing doses (from 125 to 2,000 micrograms/min) of adenosine was given to 20 patients. Adenosine infusion was then repeated after intrailiac infusion of either bamiphylline or saline solution. In 14 other patients with angina, increasing doses of adenosine (from 108 to 1,728 micrograms/min) were infused into the left coronary artery. Adenosine infusion was then repeated after the intravenous infusion of either bamiphylline or placebo. Coronary blood flow velocity was monitored by a Doppler catheter. Data relative to pain severity are expressed as median and all other data as mean value +/- 1 SD. RESULTS: Bamiphylline prolonged the time to pain onset caused by the intrailiac adenosine infusion from 444 +/- 96 to 749 +/- 120 s (p < 0.001) and reduced pain severity from 45 to 24 mm (p < 0.01). After placebo infusion, the time to pain onset and pain severity were similar to that of baseline (428 +/- 112 vs. 430 +/- 104 s, p = 0.87 and 44 vs. 43 mm, p = 0.67, respectively). Bamiphylline prolonged the time to pain onset caused by intracoronary adenosine infusion from 519 +/- 128 to 603 +/- 146 s (p < 0.01) and reduced pain severity from 58 to 28 mm (p < 0.02). After placebo infusion, the time to pain onset and pain severity were similar to that at baseline (542 +/- 87 vs. 551 +/- 79 s, p = 0.14 and 55 vs. 50 mm, p = 0.61). Maximal coronary blood flow velocities before and after bamiphylline administration were similar (47 +/- 22 vs. 49 +/- 24 cm/s, p = 0.36) as well as before and after placebo administrtion (40 +/- 20 vs. 41 +/- 20 cm/s, p = 0.07). CONCLUSIONS: Bamiphylline reduces adenosine-induced muscular and cardiac pain but does not affect adenosine-induced coronary vasodilation. These findings indicate that at the dose used in this study, bamiphylline does not detectably block vascular A2-receptor-mediated adenosine effects in humans, which suggests that the muscular and cardiac algogenic effects of adenosine are mediated mainly by A1 receptors.

Adenosine↗
PubMed1995

Thrombogenesis in acute coronary syndromes.

It is well-established that intracoronary thrombosis, which may be associated with plaque fissure and enhanced coronary vasoconstriction, is the immediate cause of a sudden impairment of regional myocardial perfusion, which is transient in unstable angina and is, eventually, irreversible in acute myocardial infarction. It is also well-known that increased platelet reactivity, increased procoagulant activity, and reduced endogenous fibrinolysis are risk factors for acute coronary events. Nevertheless, the primary causes responsible for sudden intracoronary thrombosis and for coronary vasoconstriction causing acute coronary syndromes are still largely speculative. Recent studies have shown activated inflammatory cells both in the coronary arterial wall and in the systemic circulation of patients with unstable angina. Furthermore, the intensity of the inflammatory response is correlated with an adverse prognosis. This inflammatory component may have important pathogenetic and prognostic roles because an outburst of inflammatory cytokines has the potential to increase the sensitivity of platelets to agonists, to turn the anticoagulant and vasodilator physiological properties of the endothelium into procoagulant and vasoconstrictor properties, and to cause plaque fissure by the release of proteolytic enzymes.

Acute Disease↗
PubMed1995

Catheter ablation of left accessory atrioventricular connections: the transseptal approach.

BACKGROUND: In the past few years, there has been a relative explosion of activity in the realm of interventional cardiology. The high rate of success of radiofrequency energy ablation have transformed catheter ablation from an investigational procedure into the first-line therapy for symptomatic Wolff-Parkinson-White syndrome. Radiofrequency catheter ablation for preexcitation syndrome is commonly based on a ventricular approach. Such an approach might be associated with the risk of prolonged arterial catheter manipulation, retrograde left ventricular catheterization, and production of multiple, potentially arrhythmogenic, ventricular lesions created during ablation. Potential risks can be avoided using atrial insertion ablation procedures. The transseptal procedure that was developed in the 1950s and 1960s as a diagnostic procedure and then shelved in the 1970s and early 1980s has now come back into prominence as a therapeutic technique in the treatment of valvular heart disease, and then in the ablation of the left accessory atrioventricular connections. METHODS: Atrial aspect of mitral annulus is a relatively smooth, nonobstructed surface that simplifies catheter movement, thereby permitting rapid and accurate accessory pathway location. Although primary use of earliest endocardial retrograde atrial activation as a marker of accessory pathway atrial insertion is sufficiently accurate to permit successful ablation, direct recording of an accessory pathway potential is an important predictor of successful ablation site. Moreover, the analysis of the unipolar atrial electrogram, recorded during sinus rhythm from the tip of the ablation catheter, provides further information for localizing the atrial insertion of the accessory pathways. Shortest atrial-accessory pathway and negative delta-accessory pathway intervals have been found to be the best predictors of the successful site. RESULTS: A 90.5% success of the transseptal approach on an overall population of 328 patients, higher for overt than for concealed pathways, is comparable with the results of the retrograde. Complications are 0.5%. CONCLUSION: In conclusion, the transseptal approach for ablation at the atrial site is very safe and highly effective, and avoids prolonged arterial cannulation and catheter manipulation in the ascending aorta and left ventricle.

Catheter Ablation↗
PubMed1995

Differences in vasodilatory response to dipyridamole between patients with angina and normal coronary arteries and patients with successful coronary angioplasty.

BACKGROUND: Previous studies reported a reduced coronary blood flow reserve, assessed by the intravenous administration of dipyridamole, in patients with angina and normal coronary arteries, and early after successful coronary angioplasty, which suggests the presence of small coronary vessel dysfunction. This study aimed to establish whether the mechanisms of small coronary vessel disease in these two groups of patients are similar. METHODS: The effects of the intracoronary infusion of adenosine and dipyridamole (maximum dose 2.7 and 7.5 mg/min, respectively) on coronary blood flow velocity were assessed in 11 patients with angina and normal coronary arteries (group A) and in 12 patients immediately after successful coronary angioplasty (group B) using a 0.018" Doppler wire. RESULTS: Baseline coronary blood flow velocity was significantly higher in group B than group A (34 +/- 14 versus 19 +/- 8 cm/s; P = 0.001). In group A, coronary blood flow velocity was higher during adenosine than dipyridamole infusion (74 +/- 17 versus 58 +/- 21 cm/s; P < 0.001), whereas in group B velocities were similar (85 +/- 30 versus 78 +/- 32 cm/s; NS). CONCLUSIONS: In patients with angina and normal coronary arteries, a maximal dose of adenosine causes a greater coronary dilation than that of dipyridamole. Given that dipyridamole operates mainly through an inhibition of adenosine re-uptake, it can only dilate the arteriolar segments exposed to endogenous adenosine. Therefore, the lower response to dipyridamole than to exogenous adenosine observed in patients with angina and normal coronary arteries suggests an impairment of the pre-arterioles that are not influenced by endogenous adenosine, resulting in a limited flow-mediated dilation in response to arteriolar dilation. Such an impairment is not apparent immediately after successful coronary angioplasty, where the most obvious abnormality is an increase of baseline coronary blood flow velocity.

Adenosine↗
PubMed1995

Risk factors in patients with different clinical and angiographic manifestations of ischemic heart disease.

In patients who present with unheralded myocardial infarction both the severity and the extent of coronary atherosclerosis appear to be less than that in patients with chronic stable angina, thus suggesting that, in the latter, protective factors may prevent or delay the evolution towards acute coronary syndromes. Therefore, risk factors were compared in 88 consecutive patients (73 men; mean age 56 +/- 9 years) with unheralded myocardial infarction and a single, discrete, > 70% stenosis in the proximal right, left circumflex or left anterior descending coronary artery (Group 1) and in 55 consecutive patients (46 men; mean age 58 +/- 9 years with chronic stable angina and multiple, diffuse, > 70% stenoses localized both in the right and left coronary arteries (Group 2). Continuous data are presented as mean value +/- 1 SD, proportions as percentages. In Group 1 mean serum levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides were similar to those in mg/dl, p = 0.93 and 160 +/- 87 vs 155 +/- 76, p = 0.74, respectively) while the mean serum level of high-density lipoprotein cholesterol was higher in Group 2 (49 +/- 4 vs 46 +/- 4 mg/dl, p = 0.005). The prevalence of a positive family history of ischemic heart disease, hypertension and smoking habit were similar in the two groups, while the prevalence of diabetes mellitus was higher in Group 2 (29 vs 6%, p = 0.001). Thus, in patients with otherwise similar coronary risk factors, higher levels of high-density lipoprotein cholesterol and diabetes mellitus appear to be associated with a reduced tendency of coronary atherosclerosis to cause acute coronary syndromes.

Aged↗
PubMed1995

Early postoperative myocardial ischemia after coronary artery bypass grafting. Detrimental effects of nitroglycerine infusion.

This study was aimed at assessing the incidence and mechanisms of myocardial ischemia early after coronary artery bypass grafting and the effects of treatment with nitroglycerine. The electrocardiogram of 35 patients (29 males and 6 females, mean age 61 +/- 8 years) with stable angina and multivessel coronary disease, was monitored continuously for 24 hours after uncomplicated coronary artery bypass grafting. Patients were randomized to receive nitroglycerin infusion or placebo. Fourteen of the 35 patients (40%) had 24 transient ischemic episodes (mean duration 11.8 +/- 3.5 min; range 6-20 min with ST segment elevation in 6, ST segment depression in 7 and both ST segment elevation and depression in 1. Seventy-five per cent of the ischemic episodes occurred within the first 6 postoperative hours. The mean ejection fraction prior to surgery and the mean number of stenosed vessels and of the implanted grafts were similar in patients with and without postoperative ischemia (57 +/- 5 vs 57 +/- 6%, p = 0.86; 2.7 +/- 0.5 vs 2.8 +/- 0.4, p = 0.52 and 3.0 +/- 0.9 vs 3.2 +/- 0.7, p = 0.51, respectively) as well as total bypass time and cross-clamp time (123 +/- 38 vs 124 +/- 18 min, p = 0.89 and 67 +/- 20 vs 70 +/- 14 min, p = 0.68, respectively). The values of heart rate and systolic blood pressure at the onset of the ischemic episodes were similar to those recorded 15 min before (103 +/- 16 vs 106 +/- 18 b/min, p = 0.36 and 119 +/- 12 vs 121 +/- 14 mmHg, p = 0.48). Ischemic episodes were recorded in 9 of the 16 patients (56%) randomized to receive nitroglycerine and in 5 only of the 19 patients (26%) randomized to receive placebo (p = 0.05). Thus, transient ischemic episodes occurring early after coronary artery bypass grafting are not preceded by an increase in myocardial oxygen consumption; they appear to be due, therefore, to a primary reduction in coronary blood flow. Treatment with nitroglycerine is associated with a higher prevalence of ischemic episodes, thus suggesting that myocardial ischemia is unlikely to be caused by spasm of large epicardial vessels or grafts. Myocardial ischemia may be caused, instead, by extracorporeal circulation-induced alterations enhanced by the hypotensive effects of nitroglycerine.

Aged↗