Oren Agranat

Fate of nonobstructive aneurysmatic coronary artery disease: Angiographic and clinical follow-up report

The incidence of coronary aneurysmatic dilatation without coronary stenosis is rare, and the clinical course of such an entity is unknown. We present five adult patients, four men and one woman, with such an anatomic finding. The age range was 44 to 60 years. In four patients the aneurysmatic dilatations involved multiple coronary sites. The clinical course in all five patients was suggestive of coronary insufficiency. Despite no obstructive disease, two of the patients developed transient ischemic ECG changes accompanied by chest pain, and another two patients demonstrated ischemic exercise nuclear ventriculography response. In time, all five patients developed acute myocardial infarction and recatheterization revealed complete occlusion of a previously nonstenosed aneurysmatic vessel. More information is needed in order to guide therapy. However, prevention of thrombus formation and close follow-up is highly recommended.

Impact of Atrioventricular Compliance on Pulmonary Artery Pressure in Mitral Stenosis An Exercise Echocardiographic Study

BackgroundThe decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (Cn). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that Cn is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. Methods and ResultsTwenty patients with mitral stenosis were examined by Doppler echocardiography. Cn, calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43±12 mm Hg at rest to 71±23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between Cn and exercise PAP (r =−0.85). Patients with a low compliance were more symptomatic (P <0.025). Catheter- and Doppler-derived values for Cn, determined in 10 cases, correlated well (r =0.79). ConclusionsCn, which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low Cn represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.

Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: Clinical and angiographic study☆

OBJECTIVES This study was undertaken to test the hypothesis that early inversion of T waves after thrombolytic therapy for acute myocardial infarction predicts patency of the infarct-related artery with high Thrombolysis in Myocardial Infarction (TIMI) perfusion flow and better in-hospital outcome. BACKGROUND Although numerous studies have demonstrated a strong association between early resolution of ST segment elevation after acute myocardial infarction and successful thrombolysis, little is known about early changes in T waves after thrombolytic therapy. METHODS Ninety-four consecutive patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator (rt-PA) were studied with admission and predischarge radionuclide ventriculography and with coronary angiography within 72 h of admission. Patient stratification was based on the presence or absence of early (within 24 h) T wave inversion. RESULTS Early T wave inversion was associated with a higher patency rate of the infarct-related artery (90% vs. 65%, p < 0.02) and less severe residual stenosis ([mean +/- SD] 73 +/- 27 vs. 83 +/- 22, p = 0.06), and when only TIMI perfusion grade 3 was considered, the difference was even greater (77% vs. 41%, p < 0.001). Patients with early inversion of T waves had a lower peak creatine kinase value ([mean +/- SD] 678 +/- 480 vs. 1,076 +/- 620, p < 0.01), and although a similar percent of patients with and without early T wave inversion had a normal ejection fraction (> or = 55%) on admission, a higher percent of patients with early inversion had a normal ejection fraction at hospital discharge (71% vs. 44%, p < 0.03). Early T wave inversion anticipated a more benign in-hospital clinical course with a lower incidence of adverse cardiac events (10% vs. 33%, p < 0.02). CONCLUSIONS Early inversion of T waves in patients with acute myocardial infarction treated with thrombolytic therapy suggests patency of the infarct-related artery, better perfusion grade and left ventricular function and a more benign in-hospital course.

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion.

OBJECTIVES We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion. BACKGROUND Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself. METHODS We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (< or =12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation. RESULTS Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083+/-585 IU/ml vs. 1,950+/-1,216, p < 0.01; and inferior infarction: 940+/-750 IU/ml vs. 1,350+/-820, p=0.18) and better left ventricular ejection fraction (anterior infarction: 49+/-8, vs. 44+/-8, p < 0.01; inferior infarction: 56+/-12 vs. 51+/-10, p=0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01). CONCLUSIONS Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion.

Subclavian Coronary Steal Syndrome: An Obligatory Common Fate between Subclavian Artery, Internal Mammary Graft and Coronary Circulation

The long-term patency of the left internal mammary artery (IMA) has made it the preferred conduit for myocardial revascularization. The proximal segment of the subclavian artery becomes functionally connected to the coronary circulation as a result of IMA implantation during coronary artery bypass surgery. The subclavian coronary steal syndrome results from stenosis in the left subclavian artery proximal to the IMA, compromising blood flow to the myocardium. We describe 7 patients, aged 55–75 years, 1.7–10.5 years after coronary bypass who presented with recurrent angina due to subclavian artery stenosis. The IMA graft was found open in each patient. A true steal mechanism was not demonstrated, casting doubt on the syndrome’s traditional name. Angioplasty and stenting of the subclavian artery resulted in the immediate disappearance of angina and continuous benefit at a follow-up of 3–32 months. The subclavian coronary steal syndrome, although rare, is a severe condition readily treated by angioplasty and stenting.

Frequency and Clinical Significance of Anomalous Origin of Septal Perforator Coronary Artery

Abstract The reported incidence of anomalous origin of coronary arteries ranges from 0.6 to 1.2%. 1–3 The most common variations reported are anomalous origin of the circumflex and conal arteries and, less often of the left anterior descending and right coronary arteries. 1–5 Anomalous origin of first septal perforator coronary artery (ASA) has been reported in only 3 living patients, 3 and its clinical significance is not known. We reviewed 2,100 consecutive angiograms from adult patients to determine the incidence of an ASA and its role as a collateral vessel in patients with obstructive coronary heart disease.

Left main coronary artery atresia : Extremely rare coronary anomaly in an asymptomatic adult and an adolescent soccer player

Left main coronary artery atresia is a very rare coronary anomaly with only 33 cases reported in the literature, of whom only 1 patient is asymptomatic. Pediatric patients are usually very symptomatic early in life (dyspnea, syncope, failure to thrive, ventricular tachycardia, and sudden death), whereas adult patients begin showing symptoms (angina or sudden death) only at an advanced age. Given the high risk related to the presence of left main coronary artery atresia, and in view of the good results obtained by coronary artery bypass surgery, coronary artery revascularization should always be considered as the possible treatment of choice for establishing adequate myocardial blood flow.

Rescue Coronary Angiography after Failed Thrombolysis: A Real-Life Experience

Failed thrombolysis in acute myocardial infarction (AMI) patients is associated with a high risk of morbidity and mortality. Rescue or salvage percutaneous transluminal coronary angioplasty (PTCA) in this group of patients is still controversial. We report our experience with early emergency angiography and rescue PTCA in 27 patients who were hemodynamically unstable or had a large area of myocardium at risk after failed thrombolysis. Rescue PTCA was successful in 95% of attempted PTCA. Three patients were referred to emergency CABG. Early ‘rescue angiography’ with or without rescue PTCA after failed thrombolysis in a selected patient population, is an important tool for early risk stratification and decision-making during the hyperacute phase of AMI, while it may also serve in restoring coronary artery patency of the infarct-related artery with a high success rate.

Coronary arterioluminal communications in routine angiography.

Visualization of the left ventricular cavity from coronary arterioventricular communications is rarely encountered in routine coronary angiography. We report 14 patients, of 5,500 consecutive cardiac catheterizations, in whom these communications were evident during coronary angiography. All 14 patients had angina pectoris; in each the arterioluminal communication originated from the left anterior descending coronary artery. Two patients had evidence of anterior wall ischemia despite a normal left anterior descending coronary artery, suggesting that a possible steal phenomenon is responsible for the myocardial ischemia.

Prostaglandin E1 during angioplasty as preventative therapy for coronary restenosis.

The effect of intravenous prostaglandin E1 (PGE1) on the incidence of restenosis after elective percutaneous transluminal coronary angioplasty (PTCA) was studied in a prospective, single-blind, randomized trial of 30 patients. Group I (12 patients) received only the conventional medications before and after protocol, and group II (18 patients) received intravenous PGE1 influsion for 24 hours starting at least 2 hours before angiography after hemodynamically based titration to a mean dosage of 16 ± 3 ng/kg/min (range, 10–20 ng/kg/min). All patients received aspirin orally, beginning 24 hours before PTCA and continuing for 6 months, and intravenous heparin at 1000 U/h for 24 hours commencing with the beginning of catheterization before PTCA. Recatheterization was performed routinely at 6 months after PTCA, or earlier when clinically indicated. Angiographic evaluations were made by both visual and quantitative assessment. No significant side effects of PGE1 treatment were observed. Only 17% of patients treated by PGE1 experienced angina pectoris during 6-month follow-up period, as compared with 42% of patients who received conventional treatment (p = 0.13). Re-PTCA was more frequent in patients receiving conventional therapy than in those receiving PGE1 (42% versus 11%; p = 0.06). The use of PGE1 during PTCA was associated with 17% restenosis (both by computer and by visual evaluation) 6 months post-PTCA as compared with 33% and 50% restenosis (by computer and by visual evaluations, respectively) in the conventional group (p < 0.05). In conclusion, PGE1 appears to decrease coronary restenosis 6 months after PTCA.