Abstract
We present a case of takotsubo cardiomyopathy and demonstrate an initial elevation of microcirculatory resistance (IMR) that reduced on follow-up evaluation. This corresponded with improvements in left ventricular function. We postulate that the changes in microvascular resistance reflect favourable left ventricular microvascular remodelling. The measurement of IMR, a novel marker of microcirculatory dysfunction, provides novel insights into the pathophysiology of this condition.
1
Introduction
Takotsubo cardiomyopathy (TCM) is a recently recognised clinical entity whose underlying pathophysiology remains elusive and controversial. We present a case of TCM and highlight novel coronary physiology findings that may help to explain the underlying pathophysiology of this condition.
2
Case
A 63-year-old female with a history of recent family stressors presented with acute shortness of breath and chest pain. The electrocardiograph demonstrated acute anterior ST-segment elevation, and she was taken emergently to the catheter laboratory. Diagnostic coronary angiography demonstrated an absence of left coronary disease with an intermediate lesion in the right coronary artery (RCA), however; its myocardial supply did not extend to the left ventricular apex. Left ventriculography showed apical ballooning with akinesis of the apex, mid, and distal anterior and inferior walls with hyperkinesis of the basal segments ( Fig. 1 ). Virtual histology intravascular ultrasound (VH-IVUS) (Volcano, Inc., Rancho Cordova, CA, USA) was performed in the left anterior descending and circumflex arteries, showing mild plaque only without evidence of rupture or thin fibrous cap atheroma. An assessment of the microcirculation was then performed using the index of microvascular resistance (IMR). This technique determines the minimum achievable microvascular resistance using a temperature- and pressure-sensing guide wire (TPSG), commonly used to measure fractional flow reserve. Briefly, the technique involves the measurement of a surrogate of coronary blood flow (mean transit time) that is derived from the injection of 3 ml of room-temperature saline into a coronary artery at hyperemia to achieve three reproducible thermodilution curves. Pressure distal to a stenosis is also measured at hyperemia and is then multiplied by the mean transit time to derive IMR. High levels of IMR have been reported in acute ST-segment myocardial infarction . In our case, the IMR in the left anterior descending (LAD) artery was consistent with high microvascular resistance with an elevated value (45 U). There was also an elevation of IMR in the RCA (37 U). The patient returned 6 weeks following the initial event for further evaluation of the RCA. Repeat IMR at this time showed that microvascular resistance had fallen in the LAD (21 U) and RCA territories (24 U), coinciding with complete normalization of left ventricular function ( Fig. 2 ).
2
Case
A 63-year-old female with a history of recent family stressors presented with acute shortness of breath and chest pain. The electrocardiograph demonstrated acute anterior ST-segment elevation, and she was taken emergently to the catheter laboratory. Diagnostic coronary angiography demonstrated an absence of left coronary disease with an intermediate lesion in the right coronary artery (RCA), however; its myocardial supply did not extend to the left ventricular apex. Left ventriculography showed apical ballooning with akinesis of the apex, mid, and distal anterior and inferior walls with hyperkinesis of the basal segments ( Fig. 1 ). Virtual histology intravascular ultrasound (VH-IVUS) (Volcano, Inc., Rancho Cordova, CA, USA) was performed in the left anterior descending and circumflex arteries, showing mild plaque only without evidence of rupture or thin fibrous cap atheroma. An assessment of the microcirculation was then performed using the index of microvascular resistance (IMR). This technique determines the minimum achievable microvascular resistance using a temperature- and pressure-sensing guide wire (TPSG), commonly used to measure fractional flow reserve. Briefly, the technique involves the measurement of a surrogate of coronary blood flow (mean transit time) that is derived from the injection of 3 ml of room-temperature saline into a coronary artery at hyperemia to achieve three reproducible thermodilution curves. Pressure distal to a stenosis is also measured at hyperemia and is then multiplied by the mean transit time to derive IMR. High levels of IMR have been reported in acute ST-segment myocardial infarction . In our case, the IMR in the left anterior descending (LAD) artery was consistent with high microvascular resistance with an elevated value (45 U). There was also an elevation of IMR in the RCA (37 U). The patient returned 6 weeks following the initial event for further evaluation of the RCA. Repeat IMR at this time showed that microvascular resistance had fallen in the LAD (21 U) and RCA territories (24 U), coinciding with complete normalization of left ventricular function ( Fig. 2 ).
