Therapeutic decision-making for patients with fluctuating mitral regurgitation

Mitral regurgitation (MR) is a common, progressive, and difficult-to-manage disease. MR is dynamic in nature, with physiological fluctuations occurring in response to various stimuli such as exercise and ischaemia, which can precipitate the development of symptoms and subsequent cardiac events. In both chronic primary and secondary MR, the dynamic behaviour of MR can be reliably examined during stress echocardiography. Dynamic fluctuation of MR can also have prognostic value; patients with a marked increase in regurgitant volume or who exhibit increased systolic pulmonary artery pressure during exercise have lower symptom-free survival than those who do not experience significant changes in MR and systolic pulmonary artery pressure during exercise. Identifying patients who have dynamic MR, and understanding the mechanisms underlying the condition, can potentially influence revascularization strategies (such as the surgical restoration of coronary blood flow) and interventional treatment (including cardiac resynchronization therapy and new approaches targeted to the mitral valve)

HYBERNATING MYOCARDIUM. ANOTHER PIECE OF THE PUZZLE FALLS INTO PLACE

Revascularization of hibernating myocardium (HM) (1–5) improves or normalizes left ventricular (LV) ejection fraction (EF) and the patient’s New York Heart Association functional class (6). Allman et al. (7) have analyzed data from 24 studies involving 3,088 patients who had LVEF of 0.32 0.08 and follow-up at 25 10 months. Patients who had revascularization when compared to “medical therapy” showed that (7): 1) in those with HM, See page 969 mortality was lower (3.2% vs. 16.0 %, p 0.0001), and 2) the lower the LVEF, the greater was the reduction in mortality. In addition, the composite of subsequent myocardial infarction (MI), heart failure, and unstable angina was also lower (6.0% vs. 12.2%, p 0.001) (8). These benefits were not seen in patients without HM but who nonetheless had been revascularized (7,8). In this issue of the Journal, Ambrosio et al. (9) have presented the findings of a carefully performed study which shows that in patients with either non–Q-wave MI or no previous MI but with LV wall motion abnormality and HM, there is remodeling of the LV; that is, LV enddiastolic volume (EDV) and end–systolic volume (ESV) are increased and the LV is more spherical. Thus, they have documented that the mere presence of LV systolic dysfunction with HM can lead to LV remodeling

Hibernating myocardium - Another piece of the puzzle falls into place

Hibernating myocardium - Another piece of the puzzle falls into plac

Coronary revascularization and recovery of function: the ultimate target.

Recovery of contraction in the akinetic segments represents an important target of coronary revascularization, and the preoperative recognition of viable dyssynergic (hibernating) myocardium is a crucial point in the preoperative investigation of patients with chronically depressed left ventricular function. Dobutamine-echocardiography was utilized in 14 patients to study the contractile reserve retained by viable segments. Redistribution of thallium-201 after rest injection was also used to assess the viability of these areas. The wall motion response to dobutamine infusion predicted immediate postoperative improvement in 85 of 93 segments (sensitivity 91%) and identified 25 of 32 segments which did not exhibit early postoperative improvement (specificity 78%). Rest-redistribution of thallium-201 demonstrated high sensitivity (93%) but low specificity (44%) for predicting the early recovery of regional wall motion. When late recovery was also considered, the specificity of this method increased to 64%. Recovery of function following coronary revascularization can be predicted in patients in whom hibernating myocardium is recognized preoperatively

Stunned and hibernating myocardium: possibility of intervention.

There are several potential outcomes of myocardial ischemia. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When myocardial ischemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed hibernating myocardium. The difference between this condition and that described before, i.e., prolonged ischemia, which results in further damage on reperfusion, is, most likely, related to residual coronary flow. In the hibernating myocardium, which is always supplied by a narrow coronary artery, blood flow is not low enough to cause progression toward tissue necrosis, but it is low enough to cause pH changes that, in turn, are responsible for the downregulation of myocardial contractility. The level of underperfusion is sufficient to maintain aerobic metabolism of the quiescient myocardium as demonstrated by the absence of lactate and creatine phosphokinase release. There are no doubts that revascularization is essential for hibernated myocardium, and the clinical goal to achieve is the possibility of accurately distinguishing viable from infarcted tissue. A third possible outcome of myocardial ischemia is a postischemic ventricular dysfunction or myocardial stunning. This term describes a transient mechanical dysfunction that persists on reperfusion after a short period of ischemia, despite the absence of irreversible damage. There are numerous clinical conditions in which stunning might manifest.(ABSTRACT TRUNCATED AT 250 WORDS