Left main coronary artery aneurysm.

Left main coronary artery aneurysms (LMCA) are usually asymptomatic and are rarely encountered during coronary angiography. The most serious complications include coronary thrombosis, acute myocardial infarction and sudden death. Atherosclerosis is the most common cause, although several autoimmune diseases and congenital abnormalities have been associated with the presence of coronary aneurysms. The case of a symptom-free 63-year-old man with a giant LMCA and severely ectatic coronary arteries is presented.

Heart transplantation in a low-organ-donation environment: a single center experience.

OBJECTIVE: Heart transplantation is the "gold standard" for treating patients in end-stage heart failure who satisfy strict selection criteria. However, infrequent transplant performance, eg, less than nine per year, may be associated with suboptimal results. METHODS: We reviewed our 13-year clinical experience (1996-2008) with 73 orthotopic heart transplants performed under strict selection criteria and followed closely thereafter at the only accredited center in Greece, a country with an annual rate of only seven donors per million population. RESULTS: Low perioperative (5.47%) and long-term (7.5%) mortality rates were responsible for a 94% survival rate in the first year, 92% at five years, and 70% at ten years-similar to those reported worldwide-along with excellent functional recovery. CONCLUSION: Strict recipient and donor selection criteria, combined with a rigorous multidisciplinary follow-up, yield excellent results despite the existing shortage of available grafts.

Dissociation of stress-activated protein kinase (p38-MAPK and JNKs) phosphorylation from the protective effect of preconditioning in vivo.

The aim of the present study was to examine and compare the role of the stress-activated protein kinases in ischemic and stretch-induced preconditioning. A model of anesthetized rabbits was used, and the preconditioning protocol included one or three cycles of short ischemia/reperfusion, or short mechanical stretch with acute pressure overload without or with the addition of the stretch blocker gadolinium. Infarct size was determined after 2h reperfusion and p38 MAPK and JNKs phosphorylation was determined after 20 min of prolonged ischemia. Preconditioning stimuli were equally effective in reducing the infarct size (14.2+/-3.4%, 12.9+/-3.0%, 15.9+/-3.3%, P<0.01 vs control). The addition of the stretch channel blocker gadolinium abrogated the effect of stretch preconditioning only, without any effect on ischemic preconditioning. Comparing p38-MAPK and p46/p54 JNKs phosphorylation in the ischemic and non-ischemic regions of the heart at the time of sustained ischemia, activation was observed in the ischemic or mechanically preconditioned groups compared with the control. The addition of gadolinium abolished this activation. The above results indicate that the phosphorylation of p38-MAPK and p46/p54 JNKs is increased in preconditioning but this effect can be dissociated from the protective effect of ischemic preconditioning. Activation of the stress-activated protein kinases may be related to the increased contracture, a characteristic of ischemic preconditioning.

Heart failure in beta thalassemia: a 5-year follow-up study.

PURPOSE: To evaluate the survival of patients with beta thalassemia and heart failure who were treated with iron chelation therapy. SUBJECTS AND METHODS: Fifty-two consecutive patients with beta thalassemia and heart failure were followed in a prospective 5-year study. All patients underwent a full clinical examination with chest radiograph, electrocardiogram, and echocardiographic investigation performed at 6-month intervals or when a new symptom developed. RESULTS: Of the 52 patients (mean [+/- SD] age, 24 +/- 5 years), 25 (48%) survived 5 years after the onset of heart failure. Forty-three patients had left-sided heart failure, and 9 had right-sided heart failure. Those with left-sided heart failure were younger at presentation with heart failure (22 +/- 4 years vs. 31 +/- 6 years; P <0.001), had lower ejection fractions (36% +/- 9% vs. 64% +/- 10%; P <0.001), and had a lower mean serum ferritin level (3355 +/- 1241 ng/mL vs. 6,397 +/- 1,613 ng/mL; P <0.001). CONCLUSION: The 5-year survival rate in patients with beta thalassemia with heart failure was greater than previously reported. There are clinical characteristics that may make patients more likely to develop left- or right-sided heart failure.

Serial evaluation of coronary flow reserve by transesophageal doppler echocardiography after angioplasty of proximal left anterior descending coronary artery: a 6-month follow-up study.

BACKGROUND: Coronary flow reserve can be estimated by transesophageal Doppler echocardiography (TDE). OBJECTIVE: To evaluate the coronary flow reserve by TDE, serially over 6 months' follow-up, after successful percutaneous transluminal coronary angioplasty (PTCA) of proximal left anterior descending coronary artery (LADA). METHODS AND RESULTS: We performed TDE examination of 30 patients (mean age 55 +/- 9 years) 72 h, 3 months, and 6 months after PTCA of LADA. Selective angiography of LADA was repeated 72 h and 6 months after PTCA of LADA. Velocity of flow in LADA was measured before and 2 min after cessation of intravenous infusion of dipyridamole (0.56 mg/kg in 4 min). The dipyridamole: rest mean diastolic velocity ratio was considered as an index of coronary flow reserve (CFR). For 20 of 21 patients with CFR > 2 there was no restenosis, whereas coronary angiography revealed restenosis in eight of nine patients with CFR < 2. The sensitivity was 88.9% and the specificity was 95.2%. For the 21 patients without restenosis mean CFR was 2.1 +/- 0.1 72 h after PTCA, had increased to 3.1 +/- 0.3 (P < 0.0001) 3 months after PTCA, and remained stable thereafter (3.0 +/- 0.9). CONCLUSION: CFR after PTCA of proximal LADA can be evaluated serially by transesophageal Doppler echocardiography. CFR of LADA in patients without restenosis is increased 3 months after PTCA and remains stable thereafter.

Preconditioning limits myocardial infarct size in hypercholesterolemic rabbits.

BACKGROUND: Hypercholesterolemia predisposes to coronary artery disease and causes endothelial dysfunction; some reports suggest that endothelial derived substances are involved in ischemic preconditioning. OBJECTIVE: Our aim was to examine the possibility that preconditioning maybe attenuated in a clinically relevant animal model of hypercholesterolemia with atherosclerosis. METHODS: Male rabbits were fed with cholesterol enriched diet and then divided into two groups (A and B) without and with preconditioning, respectively. A second series of rabbits fed a normal diet were similarly divided into two groups (C and D) without and with preconditioning, respectively. All the animals were subjected to 30 min ischemia and 180 min reperfusion. Blood samples were collected for cholesterol assessment; arterial and heart samples were harvested at the end for histopathological examination. Infarct (I) and risk areas (R) were delineated with Zn-Cd particles and TTC staining. RESULTS: Cholesterol in groups A and B was 58.3+/-8.7 mg% at baseline and 1402+/-125 mg% at 8 weeks (P<0.0001) and in groups C and D 57.5+/-5.8 mg% before the surgical procedure. I/R% was 39. 3+/-6.3% in group A, 16.7+/-3.9% in B (P<0.01), 41.4+/-7.5% in C and 10.8+/-3.3% in D (P<0.01). CONCLUSION: We conclude that preconditioning is unlikely to be attenuated by hypercholesterolemia.

Enhanced protection of heat shock in myocardial infarction: inhibition of detrimental effect of systemic hyperthermia.

We have shown that isolated blood-perfused heat-stressed hearts are protected only when the blood donor animal has not been exposed to hyperthermia. Systematic hyperthermia results in larger infarction of both isolated control and heat-stressed hearts. In this study we investigated whether indomethacin inhibits in vivo the detrimental effect of hyperthermia. Male rabbits were divided into four groups, that is A(30), B(30), C(30), and D(30), representing hearts that ultimately received 30 minutes of ischemia. In a second series, rabbits were divided into groups A(45), B(45), (C45), and D(45) representing hearts that ultimately received 45 minutes of ischemia, and in a third series were divided into groups A(HSP), B(HSP), C(HSP), and D(HSP) representing animals that were heat shocked and their hearts were used to measure heat shock proteins. All the A groups (heat shocked) were subjected to 42 degrees C hyperthermia, all the B groups to the same procedure but with the addition of indomethacin (heat shocked + indomethacin), all the C groups served as controls, and all the D groups were treated with indomethacin only (control + indomethacin). Twenty-four hours later, all (30) and (45) groups were subjected to ischemia, whereas hearts from all (HSP) groups were harvested for heat shock protein measurements. When the animals were exposed to 30-minute ischemia, a significant difference in the infarcted to risk zone ratio (%I/R) was observed: A(30): 33.0 +/- 5.2, B(30): 16.1 +/- 4.4 [conferring a 51.2% reduction in infarct size, P < 0.05], C(30): 48.9 +/- 4.0, and D(30): 47.8 +/- 3.8 [P < 0.001 vs. B (30) and P < 0.05 vs. A(30)]. However, the %I/R did not differ among any of the (45) groups. Heat shock proteins themselves were seen to increase in A(HSP) and B(HSP) groups. Indomethacin enhances the beneficial effect of heat shock after 30-minute ischemia in vivo, reducing the infarct size by 51.2% in comparison with heat shock.

Intracoronary cyclic-GMP and cyclic-AMP during percutaneous transluminal coronary angioplasty.

We investigated intracoronary cyclic-guanosine monophosphate (c-GMP) levels during percutaneous transluminal coronary angioplasty (PTCA) since experimental studies have shown the endothelial origin of c-GMP production. Intracoronary c-GMP and cyclic adenosine monophosphate (c-AMP) were measured during coronary angioplasty in 24 patients with chronic coronary artery disease. Four coronary blood samples were taken through a catheter from the coronary artery the first sample before coronary angiography and the other three from distal to coronary obstruction, as follows: before the balloon inflation, at the maximum inflation and 5 min after restoration of coronary flow. c-GMP increased from 7.9 +/- 1.0 pmol/ml and 7.5 +/- 0.9 pmol/ml before angiography and balloon inflation to 11.1 +/- 1.3 pmol/ml at the maximum inflation (P < 0.01), with a trend to decrease 5 min after the end of the intervention (9.5 +/- 1.0 pmol/ml, P: NS). Intracoronary c-AMP levels remained almost unchanged. Five venous samples were taken to measure c-AMP before coronary angiography, before PTCA, and 5 min, 2 h and 24 h after PTCA. c-AMP values 2 and 24 h after PTCA (17.8 +/- 1.7 pmol/ml and 17.5 +/- 1.7 pmol/ml, respectively) were lower than the highest value (22.1 +/- 2.1 pmol/ml) found 5 min after PTCA, (P < 0.001). c-GMP increases distal to coronary obstructive lesion during PTCA at the time of balloon inflation, while c-AMP remains unchanged. c-AMP rises in venous circulation only. PTCA stimulates the mechanism of c-GMP release, while systemic c-AMP increase seems to be related to the stress occurring during catheterisation and PTCA.

The effectiveness of beta-blockade and its influence on heart rate variability in vasovagal patients.

The aim of this study was to assess the effectiveness of chronic medical treatment with oral propranolol and its influence on heart rate variability in patients with vasovagal syndrome. A spectral frequency domain analysis was used for the estimation of heart rate variability characteristics. Thirty-six patients, mean age 49 +/- 17 years, with a history of recurrent syncope and positive tilt testing were involved in the study. All patients received oral propranolol (five patients also had a dual chamber inhibited DDI pacemaker implanted) for a mean time 12 +/- 6 months. One patient complained of syncope during this follow-up. The tilt test repeated in 29 patients during follow-up was negative in 28. In 20 patients treatment was discontinued for 4 days and a new tilt test was then performed. Eleven of these 20 patients (55%) had a positive test (P < 0.001 compared with the group in which treatment was continued). In the group of 11 patients in whom the tilt test became positive again after medical treatment had been withdrawn (mean age 43 +/- 20 years) and in 11 asymptomatic controls (mean age 52 +/- 19 years), with no history of syncope and negative tilt testing, the heart rate variability was assessed. The increase in the low frequency component from rest to the maximum value of heart rate variability during tilt testing was higher in the vasovagal group than in the controls (2.6 +/- 1.2 vs 1.5 +/- 0.7 P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Increased response of diastolic blood pressure to exercise in patients with coronary artery disease: an index of latent ventricular dysfunction?

OBJECTIVE: To determine whether an abnormal response of diastolic blood pressure during treadmill exercise stress testing correlated with the number of obstructed vessels and with left ventricular systolic function in patients with coronary artery disease. DESIGN: Diastolic blood pressure was measured invasively during exercise stress testing and coronary angiograms and left ventriculograms were obtained at rest in patients with coronary artery disease. The abnormal (> or = 15 mm Hg) diastolic blood pressure response was compared with the number of obstructed coronary arteries and with left ventricular systolic function. SETTING: Two tertiary referral centres. PATIENTS: 50 consecutive patients (mean age 57 years) with coronary artery disease. MAIN OUTCOME MEASURES: The increase in diastolic blood pressure during exercise and its correlation with the appearance and disappearance of ST segment deviation, resting left ventricular systolic function, and the number of obstructed coronary arteries. RESULTS: Group 1: 10 (20%) patients (three with one, four with two, and three with three vessel coronary artery disease) (mean (SD) age 54.7 (12) years) had an abnormal diastolic blood pressure response that appeared 1.2 (0.3) min before ST segment deviation and became normal 0.9 (0.3) min after the ST segment returned to normal. Group 2: 40 (80%) patients (12 with one, 16 with two, and 12 with three vessel coronary arteries disease) (aged 56.8 (8.2) years) had a normal diastolic blood pressure response to stress testing. The ejection fraction (46.3 (5)%) and cardiac index (2.6 (0.1) 1/min/m2) in group 1 were less than in group 2 (61.6 (4.2)% and 3.8 (0.3) 1/min/m2 respectively, p < or = 0.001). The end systolic volume was greater in group 1 than in group 2: 38.7 (0.7 ml/m2 v 28.2 (2.1) ml/m2, p < or = 0.001. CONCLUSION: In patients with coronary artery disease an abnormal increase in diastolic blood pressure during exercise stress testing correlated well with left ventricular systolic function at rest but not with the number of obstructed coronary arteries. The abnormal response of diastolic blood pressure probably reflects deterioration of myocardial function.

Heart rate variability in patients with vasovagal syndrome.

The aim of this study was to assess the heart rate variability in patients with vasovagal syndrome (VVS). Heart rate variability was expressed as: (1) the standard deviation (SD) of the mean RR interval; and (2) the SD as a percentage of the mean RR interval (%SD). Heart rate variability was measured in VVS patients and compared with control individuals. Eighteen patients (mean age 50 +/- 14 years) with a history of recurrent syncope and positive tilt testing were included in the study. Fifteen asymptomatic individuals (mean age 53 +/- 13 years) with no history of syncope and negative tilt testing were used as a control group. The SD and %SD (39 +/- 38 and 5 +/- 4 msec) in the VVS group were statistically higher at the tenth minute of tilt testing than in the control group (20 +/- 14 and 2.5 +/- 1.8 msec, P = 0.03 and P < 0.05, respectively). The mean RR interval (mean heart rate) was shorter after the 15th minute of tilt testing in the VVS group than in the control group (RR-VVS 687 +/- 136 msec, RR-control 801 +/- 131 msec, P < 0.05). It is concluded that heart rate variability, as expressed by the SD of the mean RR interval, and the SD as a percentage of the mean RR interval (%SD) are significantly higher in VVS patients than in control asymptomatic individuals.