Normal Epicardial Coronary Arteries Research Articles

Diagnostic performance of ultrasonic tissue characterization for subendocardial ischaemia in patients with hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) patients often develop left--ventricular subendocardial ischaemia, a cause of chest symptoms, despite normal epicardial coronary arteries. The aim of this study was to examine whether ultrasonic tissue characterization or late gadolinium enhancement on cardiac magnetic resonance imaging can detect subendocardial ischaemia in patients with HCM. Subendocardial ischaemia was quantified on exercise Tc-99m tetrofosmin myocardial scintigraphy in 29 non-obstructive HCM patients with asymmetric septal hypertrophy. Ultrasonic tissue characterization using cyclic variation of integrated backscatter (CV-IB) and late gadolinium enhancement on cardiac magnetic resonance imaging were analysed separately in the right halves and the left halves of the ventricular septum in relation to subendocardial ischaemia. Subendocardial ischaemia was identified in 17 (59%) patients. The ratio of CV-IB in the right-to-left halves of the ventricular septum was significantly higher in patients with subendocardial ischaemia (1.19 ± 0.10) than those without (0.84 ± 0.10, P = 0.04). The optimal cutoff for the detection of subendocardial ischaemia was the ratio of CV-IB >1.0, with a sensitivity of 80%, specificity of 71%, and accuracy of 76%. On the other hand, late gadolinium enhancement was not associated with subendocardial ischaemia in our cohort. Ultrasonic tissue characterization using CV-IB separately in the right and left halves of the ventricular septum, but not late gadolinium enhancement on magnetic resonance imaging, provided useful information in detecting subendocardial ischaemia in patients with HCM. Ultrasonic tissue characterization may be useful in selecting patients who will benefit from medications to relieve chest symptoms.

Simultaneous Positron Emission Tomography/Magnetic Resonance Imaging Identifies Sustained Regional Abnormalities in Cardiac Metabolism and Function in Stress-Induced Transient Midventricular Ballooning Syndrome

A 70-year-old white woman with a history of hyperlipidemia, hypertension, and former smoking and a family history of premature coronary artery disease presented with acute substernal chest pain. She complained of progressive exertional dyspnea during the preceding weeks and of being under personal stress during this time. Her initial ECG showed ST-segment elevation of a maximum 0.2 mV and a reduced R-wave progression in the anteroseptal leads (V1–3). Her troponin T level was moderately elevated (0.3 ng/mL), with normal creatine kinase (CK) and CK-myocardial band (CK-MB) fraction. Cardiac catheterization was performed and showed angiographically normal epicardial coronary arteries. However, the left ventriculogram demonstrated midventricular dilatation and akinesis with a hypercontractile apex and base compatible with midventricular ballooning syndrome, a variant of Takotsubo cardiomyopathy (TTC) (Figure 1A and 1B and Movie I in the online-only Data Supplement). Transthoracic echocardiographic monitoring during the next couple of days revealed no substantial changes in midventricular akinesis. Six days after the onset of symptoms, …

Plasma homocysteine is associated with ischemic findings without organic stenosis in patients with slow coronary flow

AimTo investigate the plasma concentrations of homocysteine (Hcy) in slow coronary flow (SCF) patients before and at the end of the exercise test and compare with the values of healthy controls. MethodsStudy population consisted of 41 patients with SCF [68% men, aged 49±8 years], and 41 subjects with normal epicardial coronary arteries [56% men, aged 50±9 years]. Exercise test was performed in all study participants. Blood samples were drawn at rest and immediately at the end of exercise testing after 12h of overnight fasting. ResultsThe baseline Hcy value of the SCF patients was higher than that of the control subjects (p<0.0001), and this difference continued after exercise test between the groups (p<0.0001). Median post-exercise increases in Hcy levels were higher in the SCF group than in the control group, without a significant difference (p=0.088). In the SCF group after exercise, Hcy levels in 17 patients with angina and 18 patients with ST depression were higher than those without angina and ST depression (p<0.0001 and p<0.0001, respectively). In addition, Hcy values in patients with both angina and ST depression were greater than those with either angina (p<0.05) or ST depression (p<0.05). ConclusionThe results of this study show that there is an important pathophysiologic link between the increased levels of plasma Hcy, the degree of ischemic findings, and the severity of slow flow in SCF patients.

P 20: Coronary microvascular response to a coldpressor test and cardiac autonomic neuropathy in asymptomatic type 2 diabetic patients free of coronary stenoses

The cold-pressor test (CPT) by inducing sympathetic stimulation and a subsequent rise in myocardial oxygen demand is expected to induce an increase in coronary blood flow and a dilation of normal epicardial coronary arteries. The aim of this study was in type 2 diabetic patients (T2Ds) free of coronary stenoses to analyse the influence of cardiac autonomic neuropathy (CAN) on the coronary response to CPT measured with a non invasive method based on trans-thoracic echography-doppler (NCT00685984). We prospectively screened 118 T2Ds, without any cardiac history and fulfilling the criteria of the French guidelines, for silent myocardial ischemia (SMI: abnormal stress myocardial scintigraphy and/or echocardiography). A coronary angiography was performed in those with SMI. The distal inter-ventricular anterior coronary velocity (CV) was measured by trans-thoracic echo-doppler before and after CPT (one hand immersed in crushed ice for 120 s) in these patients and also in 16 control subjects. CAN was assessed using three standard tests (deep-breathing, lying-to-standing and Valsalva) and considered to be present if ≥2 tests were abnormal. CV before and after CPT could be measured reliably in 35 T2Ds free of coronary stenoses and with CAN function tests being performed and in all control subjects. CAN was found in 17 T2Ds. At baseline, T2Ds had higher heart rate, rate-pressure product (DP) and CV than controls (p<0.05 to <0.0001) with slightly higher levels in those with CAN. Changes after CPT/baseline in DP were lower in T2Ds with CAN than in those without CAN (26±7 vs 52±6% increase, p=0.02; 32±5% in controls) whereas changes in CV did not differ significantly in T2Ds with or without CAN and in control subjects. CV changes during CPT, i.e. related to microcirculation, correlated with DP changes in controls (r=0.45, p<0.06) and in T2Ds without CAN (r=0.65, p<0.01) but did not in those with CAN. T2Ds without evidence of coronary artery disease but with impaired vagal cardiac tests exhibit at baseline some signs of relative increase in sympathetic activity. They have a lower increase in DP after CPT which is consistent with a lower sympathetic reactivity but this increase in myocardial oxygen demand resulting from sympathetic stimulation is sufficient to increase coronary blood flow.

The impact of aging and atherosclerotic risk factors on transthoracic coronary flow reserve in subjects with normal coronary angiography.

Age may affect coronary flow reserve (CFR) especially in subjects with atherosclerotic risk factors (ARFs). The aim of this prospective, multicenter, observational study was to determine the effects of aging on CFR in patients with normal epicardial coronary arteries and ARFs. Three-hundred-thirty-five subjects (mean age = 61 years) with at least one ARF but normal coronary angiography underwent high-dose dipyridamole stress-echo with Doppler evaluation of left anterior descending artery. CFR was calculated as the ratio between hyperemic and resting coronary diastolic peak velocities. Patients were divided in age quartiles. CFR was progressively reduced with aging (1st quartile: 3.01 ± 0.69, 4th quartile: 2.39 ± 0.49, p < 0.001). This was mainly due to a gradual increase of resting velocities (1st quartile = 26.3 ± 6.1 cm/s, 4th quartile = 30.2 ± 6.4 cm/s, p < 0.001) while the reduction of hyperemic velocities remained unaffected (1st quartile = 77.7 ± 18.9 cm/s, 4th quartile = 70.9 ± 18.4 cm/s, NS). When age quartiles and ARFs were entered into a regression model, third and fourth age quartile (p < 0.0005 and p < 0.0001 respectively), left ventricular mass index (p < 0.0001), diastolic blood pressure (p < 0.001), total cholesterol (p < 0.002), fasting blood glucose (p < 0.01) and male gender (p < 0.05) were independent determinants of CFR in the whole population. Aging reduces coronary flow reserve in patients with angiographically normal coronary arteries due to a gradual increase of resting coronary flow velocity. CFR is also affected by atherosclerotic risk factors and left ventricular hypertrophy.

Correlations between myocardium selective videodensitometric perfusion parameters and corrected TIMI frame count in patients with normal epicardial coronary arteries

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Transient midventricular ballooning syndrome. An atypical presentation of takotsubo cardiomyopathy

A 72-year-old woman without cardiovascular history presented with acute substernal chest pain and dyspnoea. The electrocardiogram was normal, but the blood test analyses showed an elevated troponin T level. Emergency coronary angiography revealed normal epicardial coronary arteries, but the left ventriculogram demonstrated midventricular dilatation and akinesis with well-preserved contractility of the apex and base. The patient was diagnosed as having an atypical presentation of takotsubo cardiomyopathy. She was treated with a beta blocker and an ACE inhibitor and recovered well. A follow-up echocardiogram at 2 months showed normalization of the wall motion abnormality.

Função endotelial vascular em pacientes com fluxo coronário lento e os efeitos do nebivolol

Brachial endothelial function has been associated with coronary slow flow (CSF). Increasing blood flow to brachial artery provokes endothelium to release nitric oxide (NO) with subsequent vasodilatation. Besides its β1-blocker activity, nebivolol causes vasodilatation by increasing endothelial NO release. To assess the effects of nebivolol on vascular endothelial function in patients with CSF. Forty-six patients with CSF and 23 individuals with normal epicardial coronary arteries were examined with transthoracic echocardiography and brachial artery ultrasonography. The patients were reevaluated two months after treatment with aspirin or aspirin plus nebivolol. Patients with CSF had higher body mass index (26.5 ± 3.3 vs. 23.8 ± 2.8, p < 0.001), mitral inflow isovolumetric relaxation time (IVRT) (114.9 ± 18.0 vs. 95.0 ± 22.0 msec, p < 0.001) and lower left ventricular ejection fraction (LVEF) (63.5 ± 3.1% vs. 65.4 ± 2.2, p = 0.009), HDL-cholesterol (39.4 ± 8.5 vs. 45.8 ± 7.7 mg/dL, p = 0.003) and brachial flow-mediated dilatation (FMD) (6.1 ± 3.9% vs. 17.6 ± 4.5%, p < 0.001). There were significant correlations between FMD and the presence of CSF (r = 0.800, p < 0.001) and HDL-cholesterol (r = 0.349, p = 0.003). Among Patients with CSF, although pretreatment mean FMD values were similar (6.1 ± 4.3% vs. 6.0 ± ,6%, p = 0.917) compared to aspirin alone group, posttreatment FMD was significantly higher in patients treated with aspirin plus nebivolol (6.0 ± 3.5% vs. 8.0 ± 2.9%, p = 0.047). Treatment with nebivolol was associated with a significant increase in FMD (6.0 ± 3.6 to 8.0 ± 2.9 %, p = 0.030) whereas treatment with aspirin alone was not. Endothelial function may be impaired in both coronary and brachial arteries in patients with CSF and nebivolol may be effective in the improvement of endothelial function in patients with CSF.

Severe Coronary Tortuosity or Myocardial Bridging in Patients With Chest Pain, Normal Coronary Arteries, and Reversible Myocardial Perfusion Defects

We reviewed patients with normal or near-normal coronary angiograms enrolled in the SPAM contrast stress echocardiographic diagnostic study in which 400 patients with chest pain syndrome of suspected cardiac origin with a clinical indication to coronary angiography were enrolled. Patients underwent dipyridamole contrast stress echocardiography (cSE) with sequential analysis of wall motion, myocardial perfusion, and Doppler coronary flow reserve before elective coronary angiography. Ninety-six patients with normal or near-normal epicardial coronary arteries were screened for the presence of 2 prespecified findings: severely tortuous coronary arteries and myocardial bridging. Patients were divided in 2 groups based on the presence (false-positive results, n = 37) or absence (true-negative results, n = 59) of reversible myocardial perfusion defects during cSE and compared for history and clinical and angiographic characteristics. Prevalence of severely tortuous coronary arteries (35% vs 5%, p <0.001) or myocardial bridging (13% vs 2%, p <0.05) was 7 times higher in patients who demonstrated reversible perfusion defects at cSE compared to those without reversible perfusion defects. No significant differences were found between the 2 groups for the main demographic variables and risk factors. Patients in the false-positive group more frequently had a history of effort angina (p <0.001) and ST-segment depression at treadmill electrocardiography (p <0.001). In conclusion, we hypothesize that patients with a positive myocardial perfusion finding at cSE but without obstructive epicardial coronary artery disease have a decreased myocardial blood flow reserve, which may be caused by a spectrum of causes other than obstructive coronary artery disease, among which severely tortuous coronary arteries/myocardial bridging may play a significant role.

A case of hypertrophic cardiomyopathy with mid-ventricular obstruction (MVO) — Dramatic long-term improvement with a DDD pacemaker as assessed by diastolic paradoxical jet flow velocity

A 68-year-old woman complaining of exertional chest and back pain was referred to our hospital for a preoperative evaluation for gastric cancer. She had been treated with a β-blocker since 2002 after being diagnosed with hypertrophic obstructive cardiomyopathy (HOCM) at another hospital. The frequency of her chest and back pain episodes during stair climbing and rapid walking had increased in the previous year. Based on the studies below, a permanent DDD pacemaker with an AV delay of 80 ms was implanted at a heart rate setting of 60/min. Surgery for gastric cancer was performed uneventfully 2 months later. Continuous-waveDoppler imaging (Fig.1A)demonstratedbloodflow from the apex to the base of the left ventricle during early systole (white arrowheads) followed by high-speed blood flowduring diastole, forming biphasicwaves. The latter part of thewave is generally known as diastolic paradoxical jet flow (yellowarrows). The blood flow from the base to the apex showed triphasic waves, in which E-waves [E], A-waves [A], and high-speed bloodflow [H]were observed in the diastolic, presystolic, and early systolic phases, respectively. Color Doppler imaging of the apical four-chamber view (Fig. 1B) revealed so-called diastolic paradoxical jet flow from the apex to the base of the left ventricle (shown in blue) during diastole, with the vortex flows forming a mosaic pattern. Furthermore, as her main complaint was chest and back pain during stair climbing and rapid walking, a hemodynamic assessment was performed during exertion. After the administration of isoproterenol, the patient's heart rate increased to 110/min, and chest pain developed. In addition, her diastolic paradoxical jet flow velocity was elevated to 544 cm/s (Fig. 1C, yellow arrows), and the maximal pressure gradient increased to 119 mmHg, as estimated by continuous-wave Doppler imaging. Immediately after the start of pacing in VVI mode at a heart rate of 115/min, her diastolic paradoxical jet flow velocity decreased to less than 200 cm/s (Fig. 1D, yellow arrows). At 20 months after surgery, she is doing well without any complaints. Her diastolic paradoxical jet flow velocity was 159 cm/s at the last follow-up (Fig. 1E, yellow arrows), and her maximal pressure gradient was 10.1 mmHg, as estimated by continuous-wave Doppler imaging. The coronary cine angiogram revealed normal epicardial coronary arteries. A left ventriculogram confirmed mid-ventricular obstruction combined with an apical aneurysm, which seemed to be enlarged compared with that seen in 2002. During cardiac catheterization, simultaneous pressure measurements at the apex and base of the left ventricle demonstrated a maximal pressure gradient of 162 mmHg in the control conditions (Fig. 2, 1). Using an AV sequential pacemaker with electrodes placed in the right atrium and the right ventricle, her maximal pressure gradient was decreased from 162 mmHg to 116 mmHg (Fig. 2,2) and 20 mmHg (Fig. 2, 3) as the atrioventricular (AV) conduction delay was shortened to 120 ms and then to 70 ms, respectively. It should also be noted that the pressure gradient detected between the apex

Atypical ST-Segment—Elevation Infarction in a Patient With Bicuspid Aortic Valve

We report the case of a 51-year-old man who was admitted to our hospital with ST-segment–elevation myocardial infarction and normal epicardial coronary arteries. To the best of our knowledge, this is the first documented case of a myocardial infarction caused by intermittent occlusion of the right coronary artery by an adhering cardiac tumor on a bicuspid aortic valve. The patient presented with sudden onset of typical anginal chest pain radiating into the left arm and throat, accompanied by nausea and diaphoresis. He had no previous cardiac history, and smoking was his only cardiovascular risk factor. As a result of ST-segment elevations in the lateral precordial leads in a 12-lead surface ECG (Figure 1) and his typical clinical presentation, he was medically treated according to the ST-segment–elevation myocardial infarction guidelines by the emergency physician and directly transported to the catheterization unit in our hospital. Figure 1. Twelve-lead ECG at admission showing an ST-segment elevation in the lateral precordial leads. Myocardial infarction was confirmed by an increase in cardiac enzymes, reaching a peak of 4.2 ng/mL for high-sensitivity cardiac troponin T (normal, <0.01 ng/mL) and 171 U/L for creatine kinase-MB (normal, <25 U/mL) 6 hours after admission. Inflammation markers were negative (C-reactive protein level …

Morphologic Pattern of Late Gadolinium Enhancement in Takotsubo Cardiomyopathy Detected by Early Cardiovascular Magnetic Resonance

Takotsubo cardiomyopathy (TTC) presents clinically as an acute coronary syndrome. It is characterized by transient left ventricular wall dyskinesis-akinesis, without significant epicardial coronary lesions. Late gadolinium enhancement (LGE) sequences on cardiac magnetic resonance (CMR) allow to clarify the pathophysiology in patients with chest pain, elevated troponin, and normal epicardial coronary arteries; in patients with TTC, previous studies have shown absence of LGE. Early CMR in Takotsubo patients could show a morphological pattern of LGE improving clinical diagnosis. Between January 2005 and January 2007, 8 consecutive patients with TTC criteria underwent CMR within the first 3 days of admission. Cine, T2-weighted, and LGE images were acquired. Patient follow-up included clinical exam and imaging techniques: echocardiogram on days 3, 7, 30, and 60, and CMR at 3 months. Six patients had experienced a previous stressful situation. No significant lesions were found on coronary angiography, and wall motion improvement was noted at 15 (7-30) days. Median EFs at admission and recovery were 46.5% and 65%, respectively. Dyskinesis was midapical in 6 cases, apical in 1 case, and mid-ventricular in 1 case. Late gadolinium enhancement showed mild hyperenhancement in areas of abnormal wall motion, whereas normal segments had no contrast enhancement. On follow-up CMR, wall motion was normal without late enhancement. Early CMR in TTC demonstrates a special morphological pattern of late gadolinium uptake that might correspond to localized inflammation and edema in the affected area, suggesting diffuse microcirculation damage rather than epicardial vessel involvement.

PP-062: VASCULAR ENDOTHELIAL FUNCTION IN PATIENTS WITH CORONARY SLOW FLOW AND THE EFFECTS OF NEBIVOLOL

Background: Brachial endothelial function has been associated with coronary slow flow (CSF). Increasing blood flow to brachial artery provokes endothelium to release nitric oxide (NO) with subsequent vasodilatation. Besides its β1-blocker activity, nebivolol causes vasodilatation by increasing endothelial NO release. Objective: To assess the effects of nebivolol on vascular endothelial function in patients with CSF. Methods: Forty-six patients with CSF and 23 individuals with normal epicardial coronary arteries were examined with transthoracic echocardiography and brachial artery ultrasonography. The patients were reevaluated two months after treatment with aspirin or aspirin plus nebivolol. Results: Patients with CSF had higher body mass index (26.5 ± 3.3 vs. 23.8 ± 2.8, p < 0.001), mitral inflow isovolumetric relaxation time (IVRT) (114.9 ± 18.0 vs. 95.0 ± 22.0 msec, p < 0.001) and lower left ventricular ejection fraction (LVEF) (63.5 ± 3.1% vs. 65.4 ± 2.2, p = 0.009), HDL-cholesterol (39.4 ± 8.5 vs. 45.8 ± 7.7 mg/dL, p = 0.003) and brachial flow-mediated dilatation (FMD) (6.1 ± 3.9% vs. 17.6 ± 4.5%, p < 0.001). There were significant correlations between FMD and the presence of CSF (r = 0.800, p < 0.001) and HDL-cholesterol (r = 0.349, p = 0.003). Among Patients with CSF, although pretreatment mean FMD values were similar (6.1 ± 4.3% vs. 6.0 ±,6%, p = 0.917) compared to aspirin alone group, posttreatment FMD was significantly higher in patients treated with aspirin plus nebivolol (6.0 ± 3.5% vs. 8.0 ± 2.9%, p = 0.047). Treatment with nebivolol was associated with a significant increase in FMD (6.0 ± 3.6 to 8.0 ± 2.9 %, p = 0.030) whereas treatment with aspirin alone was not. Conclusions: Endothelial function may be impaired in both coronary and brachial arteries in patients with CSF and nebivolol may be effective in the improvement of endothelial function in patients with CSF. (Arq Bras Cardiol 2011;97(4):275-280)

Myocardial Ischemia Is Not Always Due to Epicardial Atheromatous Disease

Symptoms related to myocardial ischemia, for the most part, are due to high-grade epicardial coronary artery stenoses. However, in some instances at coronary angiography, no such lesions are seen to account for symptoms due to an imbalance between myocardial oxygen supply and myocardial oxygen demand. Thus, the finding of normal or nonobstructive epicardial coronary arteries at coronary angiography does not exclude the presence of myocardial ischemia in some patients.

Takotsubo cardiomyopathy – a clinical review

SummaryStress cardiomyopathy is characterised by reversible left ventricular dysfunction. It simulates an acute coronary syndrome (ACS), presenting with precordial pain or dyspnoea, changes of the ST segment, T wave, or QTc interval on electrocardiogram, and raised cardiac enzymes. Typical findings are disturbances of segmental contractility (apical hypokinesia or akinesia), with normal epicardial coronary arteries. The true prevalence is unknown, as the syndrome may be under-diagnosed; it is more common in postmenopausal women. There is usually a trigger in the form of physical or psychological stress. The electrocardiographic, echocardiographic, and ventriculographic changes resolve spontaneously over a variable period of time (from days to months). There are a number of pathophysiological theories, none of which has been shown to be definitive, suggesting that all of them may be involved to some extent. The prognosis is generally favourable, and recurrence is very rare.

Cardiac Contusion in a Professional Soccer Player

We report here the case of a 30-year-old professional soccer player who presented to our hospital after sustaining a blunt chest trauma. To the best of our knowledge, this is the first reported case of cardiac contusion when acute myocardial edema and subsequent chronic myocardial injury were visualized with cardiac magnetic resonance (CMR) imaging. A professional soccer player presented to our hospital with persistent chest pain and fatigue after being hit in the chest by a soccer ball during a national league game. The hospital admission was 10 hours after the accident and onset of symptoms. The patient had no medical history and no recent history of infectious disease. The initial workup revealed elevated cardiac troponin T of 0.576 μg/L (normal range, 0.00 to 0.03 μg/L) and creatine kinase-MB levels of 25.4 U/L (normal range, 0 to 25 U/L); the markers of inflammation proved to be negative (C-reactive protein level, 0.9 mg/L [normal range, 0 to 5.0 mg/L]; white blood cell count, 7.0×103/μL [normal range, 4 to 10×103/μL]). The patient underwent a performance-enhancing drug screening 8 days before the event as part of the regular doping control protocol of professional soccer players, which proved to be negative. Furthermore, the toxicology panel testing for 7 drugs (phencyclidine, barbiturates, cannabinoids, amphetamines, benzodiazepines, …

In Vitro Investigation of the Impact of Aortic Valve Stenosis Severity on Left Coronary Artery Flow

Patients with aortic valve stenosis (AS) may experience angina pectoris even if they have angiographically normal coronary arteries. Angina is associated with a marked increase in the risk of sudden death in AS patients. Only a few in vitro models describing the interaction between the left ventricular and aortic pressures, and the coronary circulation have been reported. These models were designed for specific research studies and they need to be improved or modified when other specific studies are required. Consequently, we have developed an in vitro model that is able to mimic the coronary circulation in presence of aortic stenosis. First, we have validated the model under physiological conditions. Then, we have examined and quantified the hemodynamic effects of different degrees of AS (from normal to severe AS) on the coronary flow using a model of the normal left coronary artery. In the coronary in vitro model without AS (normal valve), the amplitude and shape of coronary flow were similar to those observed in in vivo measurements obtained under physiological conditions, as described by Hozumi et al. (1998, "Noninvasive Assessment of Significant Left Anterior Descending Coronary Artery Stenosis by Coronary Flow Velocity Reserve With Transthoracic Color Doppler Echocardiography," Circulation, 97, pp. 1557-1562). The presence of an AS induced an increase in the maximum and mean coronary flow rates (97% and 73%, respectively, for a very severe AS). Furthermore, when AS was very severe, a retrograde flow occurred during systole. This study allowed us to validate our coronary in vitro model under physiological conditions, both in the absence and presence of AS. These changes could explain the fact that even if patients have angiographically normal epicardial coronary arteries, we can observe the occurrence of angina pectoris in these patients in the presence of an AS.

Noninvasive Evaluation of Membranous Subaortic Stenosis: Complimentary Roles of Echocardiography and Computed Tomographic Angiography

A 29-year-old Ethiopian woman that was referred to the Wisconsin Heart Hospital for treatment of subaortic stenosis, diagnosed 4 years earlier, in Ethiopia, using transthoracic echocardiography. Preoperative evaluation included transesophageal echocardiography, which showed severe membranous subaortic stenosis with a mean outflow gradient of 70 mmHg. Cardiac computed tomographic angiography also demonstrated a subaortic membrane, and additionally showed normal epicardial coronary arteries. The patient underwent uneventful surgical resection of the subaortic membrane without undergoing cardiac catheterization.

Persistent thebesian veins presenting with myocardial ischemia

An 82-year-old man presenting with acute coronary syndrome (exercise-induced chest pain, ST-T wave changes and troponin I 0.21 μg/L) underwent coronary angiography. The left anterior descending artery (LAD) and right coronary artery (RCA) had minor nonobstructive plaque (Figures 1A and ​and1B).1B). Left coronary injection demonstrated a capillary blush draining into the left ventricular (LV) cavity due to multiple microfistulae (Figure 1C and Video) all along the wall of the left ventricle, extensive enough to produce an LV angiogram (Figure 1D). In the absence of any myocardial tumour, ventricular hypertrophy or evidence of noncompaction (on echocardiography), this appearance suggested arterioluminal-type thebesian veins communicating between the coronary arteries and LV cavity. Figure 1 Although arterioluminal thebesian veins have a larger diameter, a network extensive enough to produce LV opacification is rare. These veins bypass myocardial capillaries and may give rise to myocardial ischemia due to coronary steal (1), because the normal circulation offers a greater resistance to flow than the fistula. Extensive communication, as in the present patient, may lead to myocardial ischemia, severe enough to cause enzyme leak. This is due to a considerable decrease in intracoronary diastolic perfusion pressure that diminishes in proportion to the size of the fistula, especially during exercise. Anginal symptoms with ST segment changes due to myocardial hypoxia confirmed by elevated coronary sinus lactate levels has been demonstrated after atrial burst pacing in patients with multiple coronary artery-LV fistulae and normal epicardial coronary arteries (2).

T-wave depletion and bradycardia possibly secondary to acute pancreatitis: Review of the literature

Acute pancreatitis has frequently been reported to be associated with transient electrocardiography changes mimicking myocardial infarction despite normal epicardial coronary arteries. Although the origin of these findings is poorly understood, suggested mechanisms have included electrolyte abnormalities, a vagally mediated reflex, coronary vasospasm, and myonecrosis because of the release of pancreatic proteolytic enzymes. We report a case of acute pancreatitis with new-onset electrocardiography changes and bradycardia despite no evidence of coronary artery disease. After resolution of inflammation in the pancreas, T-wave depletions in V1-V6 derivations in electrocardiography disappeared and the rhythm was sinus with 70/min. 201-Tl myocardial perfusion scintigraphy revealed no evidence of significant coronary artery disease.