Abstract 12885: Sleepless Nights and Squeamish Days: A Conundrum of Recurrent Myocardial Ischemia

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
H Immo Lehmann

A 63-year old Caucasian female with history of aortic valve replacement and CAD with prior drug-eluting stent placement (DES) to proximal LAD and LCX, presented as a hospital transfer with recurrent episodes of chest pain. Chest discomfort was described as severe chest pressure, radiating to bilateral upper extremities. Episodes were not associated with significant exertion and frequently occurred at night/early morning. Of note, the patient had undergone coronary angiography at the outside hospital, revealing no in-stent restenosis or new coronary lesions. Soon after the patient’s arrival in the CCU, she developed profound chest pressure, accompanied by hypotension, diaphoresis and nausea. Her 12-lead ECG revealed 2-mm ST-elevation in aVR, accompanied by ST-depression in inferior, anterior, and apical leads. Initial high-sensitivity (hs)-troponin T was 26 ng/L. She was given sublingual nitroglycerin and was started on a nitroglycerin and nicardipine infusion, with resolution of symptoms after ~30 minutes, followed by normalization of hs-troponin T. A transthoracic echocardiogram did not reveal focal left ventricular (LV) wall motion abnormalities, mild LV hypertrophy was present. Given the patients’ presentation with no in-stent restenosis or new lesions, frequent episodes of chest pain-not related to exertion with occurrence at nighttime and early morning, her presentation was deemed to be consistent with epicardial coronary vasospasm. Subsequently, the patients’ anti-anginal regimen was uptitrated to include extended-release nitrates, calcium-channel blockade, and I Na blockade. Unfortunately, she continued to have frequent episodes of profound angina, accompanied by hypotension, and significant ischemic ECG changes. This prompted us to pursue bilateral sympathectomy. Subsequently, the patient had resolution of prior symptoms. She was continued on an anti-vasospastic regimen, consisting of extended release nitrates and calcium-channel blockade. This case represents the challenging management of medication-resistant epicardial coronary artery vasospasm. As previously described, sympathectomy remains an effective therapeutic option for management in these difficult and life-threatening situations.

Hypertension ◽  
1982 ◽  
Vol 4 (3) ◽  
pp. 26-31 ◽  
Author(s):  
U. L. Hulthen ◽  
P. Bolli ◽  
F. W. Amann ◽  
W. Kiowski ◽  
F. R. Buhler

The Lancet ◽  
1996 ◽  
Vol 348 (9026) ◽  
pp. 493-497 ◽  
Author(s):  
Marco Pahor ◽  
Jack M Guralnik ◽  
Luigi Ferrucci ◽  
Maria-Chiara Corti ◽  
Marcel E Salive ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
N. B. Spath ◽  
D. M. L. Lilburn ◽  
G. A. Gray ◽  
L. M. Le Page ◽  
G. Papanastasiou ◽  
...  

Background. Manganese-enhanced MRI (MEMRI) has the potential to identify viable myocardium and quantify calcium influx and handling. Two distinct manganese contrast media have been developed for clinical application, mangafodipir and EVP1001-1, employing different strategies to mitigate against adverse effects resulting from calcium-channel agonism. Mangafodipir delivers manganese ions as a chelate, and EVP1001-1 coadministers calcium gluconate. Using myocardial T1 mapping, we aimed to explore chelated and nonchelated manganese contrast agents, their mechanism of myocardial uptake, and their application to infarcted hearts. Methods. T1 mapping was performed in healthy adult male Sprague-Dawley rats using a 7T MRI scanner before and after nonchelated (EVP1001-1 or MnCl2 (22 μmol/kg)) or chelated (mangafodipir (22–44 μmol/kg)) manganese-based contrast media in the presence of calcium channel blockade (diltiazem (100–200 μmol/kg/min)) or sodium chloride (0.9%). A second cohort of rats underwent surgery to induce anterior myocardial infarction by permanent coronary artery ligation or sham surgery. Infarcted rats were imaged with standard gadolinium delayed enhancement MRI (DEMRI) with inversion recovery techniques (DEMRI inversion recovery) as well as DEMRI T1 mapping. A subsequent MEMRI scan was performed 48 h later using either nonchelated or chelated manganese and T1 mapping. Finally, animals were culled at 12 weeks, and infarct size was quantified histologically with Masson’s trichrome (MTC). Results. Both manganese agents induced concentration-dependent shortening of myocardial T1 values. This was greatest with nonchelated manganese, and could be inhibited by 30–43% with calcium-channel blockade. Manganese imaging successfully delineated the area of myocardial infarction. Indeed, irrespective of the manganese agent, there was good agreement between infarct size on MEMRI T1 mapping and histology (bias 1.4%, 95% CI −14.8 to 17.1 P>0.05). In contrast, DEMRI inversion recovery overestimated infarct size (bias 11.4%, 95% CI −9.1 to 31.8 P=0.002), as did DEMRI T1 mapping (bias 8.2%, 95% CI −10.7 to 27.2 P=0.008). Increased manganese uptake was also observed in the remote myocardium, with remote myocardial ∆T1 inversely correlating with left ventricular ejection fraction after myocardial infarction (r=−0.61, P=0.022). Conclusions. MEMRI causes concentration and calcium channel-dependent myocardial T1 shortening. MEMRI with T1 mapping provides an accurate assessment of infarct size and can also identify changes in calcium handling in the remote myocardium. This technique has potential applications for the assessment of myocardial viability, remodelling, and regeneration.


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