Author + information
- Thach Nguyen1,2,3,
- Tran Ngoc Minh Chau2,
- Hanh Nguyen Hieu Le2,
- Nguyen Minh Tri Nhan3,
- Khanh Duong3 and
- Gianluca Rigatelli4
New onset of heart failure (HF) is an indication for investigation for coronary artery disease (CAD) In many cases, the angiogram results showed mild CAD with normal left ventricular (LV) function or mild to moderate LV dysfunction. Management was to continue medical treatment without percutaneous or surgical interventions. Whether CAD causes HF or HF causes ischemic changes on the EKG as well as the chest pain is not clear. Theoretically an elevation of the left ventricular (LV) end diastolic pressure (representing the systolic and diastolic dysfunction) might cause EKG changes suggestive of ischemia. The aim of this study was to clarify the mechanistic causes of new onset HF associated with ischemic EKG changes, chest pain in patients with patent or minimally diseased coronary arteries.
In group A, 20 patients were consecutively selected using the following criteria: (1) history of new onset of HF on presentation to the emergency room, (2) having chest pain on the index admission, (3) EKG changes indicating ischemia (ST depression or T wave inversion and no ST segment elevation), AND (4) negative coronary angiogram. Group B (control) included 15 patients with patent coronary arteries and elevated LVEDP(chronic diastolic HF). The aortic systolic (AOS), aortic diastolic (AOD), aortic mean pressure (AOM), pulse pressure, and ejection fraction (EF) were recorded. CPP using the formula CPP=AOD-LVEDP was calculated in both groups.
The results showed that both groups had a similar percentage of chest pain and SOB (p>0.05). All patients had a negative coronary angiogram. The majority of patients in group A had a higher LVEDP than the control group (B) (P<0.05). However, the AO Diastolic (AOD) pressure was lower in group A than in group B (P<0.05). In patients with elevated LVEDP and low AOD, with CPP<20mmHg, the EKG changes (type 3) with deep T wave inversion were more frequently seen in more chest and limb leads. If the CPP was between 20-30mmHg, the EKG changes were more of type 2 (mild ST depression) (p<0.5%). If the CPP > 30mmHg, there were normal EKG readings or only type 1 changes (p<0.05%). It was strongly suggested that CPP < 20mmHg was associated with chest pain and ischemia on the EKG. Once the elevated LVEDP was reduced to a lower level or when the OAD pressure improved (no more diastolic hypotension), the ST segment abnormalities improved.
In patients with HF and EKG changes suggestive of ischemia, a lower AOD could aggravate ischemia in patients with elevated LVEDP. The reason is that the coronary perfusion pressure (CPP) is the difference between AOD and LVEDP; the CPP could then decrease and cause ischemia (due to low perfusion pressure) even though the coronary arteries are patent. As result, LV dysfunction could cause ischemia in selected patients, and could be the cause of death in patients with elevated LVEDP (e.g., CAD with LV dysfunction or aortic stenosis) undergoing PCI.