During the study period, 960 patients were admitted to the intensive cardiac unit due to acute MI. Of these, 275 patients were excluded from the study: 260 patients due to non-ischemic originating mitral regurgitation or previous known mitral regurgitation, five patients due to primary mitral disease (two due to rheumatic heart disease, two due to mitral valve prolapse and one due to chest radiation), and nine patients due to secondary non-IMR-related tricuspid pathology.
Of the 685 eligible patients, 175 (25.6%) developed ischemic mitral regurgitation. Thirty-five patients were excluded due to a lack of adequate follow-up TTE exams and poor imaging quality. Thus, 134 patients were in the final study cohort (Fig. 1).
Forty patients (29%, 95% CI: 22.75–38.07%) developed functional tricuspid regurgitation (FTR) during follow-up. Demographic characteristics of the two groups revealed that patients who developed FTR were older (63.0 ± 10.4 and 57.1 ± 11.0, respectively, p < 0.05) with a high incidence of vascular disease either coronary (p < 0.006) or peripheral (p < 0.009). Failed coronary revascularization was a strong positive predictor of FTR development (p < .003). No gender difference was found between the groups. Smoking, hyperlipidemia, diabetes, and chronic kidney failure were not predictive of FTR development (Table 1).
Table 1
Characteristic
|
FTR
(n = 40)
|
No-FTR
(n = 94)
|
p-Value
|
Age
|
63.0 ± 10.4
(62.5; 45–85)
|
57.1 ± 11.0
(57; 34–89)
|
.005
|
Male
Female
|
30 (75.0)
10 (25.0)
|
76 (80.9)
18 (19.1)
|
.45
|
Smoking
|
16 (40.0)
|
59 (62.8)
|
.02
|
Chronic Kidney Failure
|
3 (7.5)
|
3 (3.2)
|
.36
|
Diabetes (types 1 and 2)
|
14 (35.0)
|
38 (40.4)
|
.56
|
Previous Coronary Catheterization
|
20 (50.0)
|
23 (24.5)
|
004.
|
Previous Bypass Surgery
|
4 (10.0)
|
3 (3.2)
|
20.
|
Peripheral vascular disease
|
5 (12.5)
|
1 (1.1)
|
.009
|
Atrial fibrillation
|
4 (10.0)
|
3 (3.2)
|
.20
|
STEMI
|
39 (97.5)
|
84 (90.4)
|
17.
|
KILLIP Score
|
|
|
|
1
|
0 (0.0)
|
0 (0.0)
|
16.
|
2
|
32 (80.0)
|
83 (88.3)
|
|
3
|
1 (2.5)
|
0 (0.0)
|
|
4
|
4 (10.0)
|
3 (3.2)
|
|
New Q on ECG
|
8 (20.0)
|
11(11.8)
|
22.
|
Infarct Area
|
|
|
.39
|
Anterior
|
20 (51.3)
|
42 (44.7)
|
|
Inferior
|
15 (38.5)
|
37 (39.4)
|
|
Lateral
|
1 (2.6)
|
4 (4.3)
|
|
Posterior
|
1 (2.6)
|
0 (0.0)
|
|
Other
|
2 (5.1)
|
11 (11.7)
|
|
Failed PCI¥
|
5 (12.5)
|
4 (4.3)
|
.03
|
Complications after PCI
|
6 (15.0)
|
6 (6.5)
|
.18
|
Culprit artery
|
|
|
|
LAD
|
65 (48.5)
|
20 (50.0)
|
45 (47.9)
|
RCA
|
45 (33.6)
|
14 (31.1)
|
31 (33.0)
|
CX
|
5 (3.7)
|
3 (7.5)
|
2 (2.1)
|
Other
|
19 ()
|
3 (7.5)
|
16 (17.0)
|
Ψ Defined as failed to perform balloon dilatation or stent implantation |
PCI, percutaneous coronary intervention |
Most patients who developed IMR had STEMI (92%). The ST-segment elevation on ECG, KILLIP class, and infarct territory was not associated with FTR development or progression (Table 1). We did not find a significant statistical correlation between the infarct-related artery involved and the development of FTR. Our analysis did not cover the correlation of multivessel disease with the development of FTR. Pulmonary arterial pressure (mean) and left ventricular systolic function as estimated by ejection fraction appeared to have a significant effect on FTR progression (p < 0.05, p < 0.02, respectively) but did not affect FTR development (p < 0.5, p < 0.54, respectively) (Table 2s and Table 3s). The distribution of incidence events and their severity among IMR patients appear to be directly and linearly linked to FTR development and progression (Fig. 2). During follow-up, the development of new FTR was observed in almost third of the patients. FTR progressed in one-fifth of patients within 1.67 years (1.8 ± SD). The development of FTR was strongly associated with elevated pulmonary arterial pressure and reduced left ventricular ejection fraction (LVEF) (Fig. 3). Atrial Fibrillation was found to be associated with TR severity 2 (χ2 = 0.96, p > .62).
Patients who developed FTR had a lower overall survival rate than patients who did not have FTR. Multivariable models to predict FTR in IMR patients indicated a statistically significant difference in survival between the two groups at the time to progression to severe FTR (Mantel Cox χ2 = 5.02, p < .025). FTR group mean survival time was 4.58 years (95% CI: 4.11–5.04 years) and the no-FTR group was 5.15 years (95% CI: 4.90–5.40 years) (Fig. 4).
FTR progression was associated with heart failure at admission. There were statistically significant greater odds of FTR progression among patients with heart failure compared to patients with no heart failure at admission (OR: 8.09; 95% CI: 3.30–19.89, p < .001).